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Paclitaxel induces human KOSC3 oral cancer cell apoptosis through caspase pathways
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作者 YU-YAN LAN TSUN-CHIH CHENG +2 位作者 YI-PING LEE CHIA-YIH WANG BU-MIIN HUANG 《BIOCELL》 SCIE 2024年第7期1047-1054,共8页
Background:Paclitaxel is a compound derived from Pacific yew bark that induces various cancer cell apoptosis.However,whether it also has anticancer activities in KOSC3 cells,an oral cancer cell line,is unclear.Methods:... Background:Paclitaxel is a compound derived from Pacific yew bark that induces various cancer cell apoptosis.However,whether it also has anticancer activities in KOSC3 cells,an oral cancer cell line,is unclear.Methods:3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide,flow cytometry,and western blotting assays were carried out to assess cell viability,subG1 phase of the cell cycle,and apoptosis-related protein expression,respectively.Results:Ourfindings indicate that paclitaxel could inhibit cell viability and increase the expression of apoptotic markers,including plasma membrane blebbing and the cleavage of poly ADP-ribose polymerase in KOSC3 cells.Also,the treatment with paclitaxel remarkably elevated the percentage of the subG1 phase in KOSC3 cells.In addition,treatment with a pan-caspase inhibitor could recover paclitaxel-inhibited cell viability.Moreover,caspase-8,caspase-9,caspase-7,and BH3 interacting domain death agonist(Bid)were activated in paclitaxel-treated KOSC3 cells.Conclusions:Paclitaxel induced apoptosis through caspase cascade in KOSC3 cells. 展开更多
关键词 PACLITAXEL Oral cancer KOSC3 cells apoptosis Caspase pathways
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Dihydroartemisinin enhances cell apoptosis in diffuse large B cell lymphoma by inhibiting the STAT3 activity
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作者 ZHENG CAO CHUNXIAO ZHOU +5 位作者 ZHIMIN WU CHUNYAN WU WEN ZHANG SHILV CHEN XINDONG ZHAO SHAOLING WU 《BIOCELL》 SCIE 2023年第5期1075-1083,共9页
Background:Dihydroartemisinin(DHA)is reported to be a potential anticancer agent,and the mechanisms underlying the effects of DHA on diffuse large B cell lymphoma however are still obscure.This study aimed to assess t... Background:Dihydroartemisinin(DHA)is reported to be a potential anticancer agent,and the mechanisms underlying the effects of DHA on diffuse large B cell lymphoma however are still obscure.This study aimed to assess the antitumor effect of DHA on diffuse large B cell lymphoma cells and to determine the potential underlying mechanisms of DHA-induced cell apoptosis.Methods:Here,the Cell Counting Kit 8 assay was conducted to study cell proliferation.We performed Annexin V-FITC/propidium iodide staining,real-time polymerase chain reaction,and western blot analysis to analyze cell apoptosis and potential molecular mechanisms.Results:The results showed that DHA substantially suppressed cell proliferation and induced cell apoptosis in vitro in a time-and concentration-dependent fashion.Moreover,STAT3 activity could be inhibited after stimulation with DHA.Conclusion:These results imply that the underlying anti-tumoral effect of DHA may increase apoptosis in diffuse large B cell lymphoma cells via the STAT3 signaling pathway.In addition,DHA might be an effective drug for diffuse large B cell lymphoma therapy. 展开更多
关键词 Diffuse large B cell lymphoma DIHYDROARTEMISININ STAT3 cell apoptosis
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Phosphatidylinositol 3-kinase/Akt pathway regulates hepatic stellate cell apoptosis 被引量:25
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作者 Yan Wang Xiao-Yu Jiang +1 位作者 Li Liu Hui-Qing Jiang 《World Journal of Gastroenterology》 SCIE CAS CSCD 2008年第33期5186-5191,共6页
AIM: To investigate the role of phosphatidylinositol 3-kinase (PI 3-K)/Akt signaling pathway in the balance of HSC activation and apoptosis in rat hepatic stellate cells (HSC). METHODS: An activated HSC cell line was ... AIM: To investigate the role of phosphatidylinositol 3-kinase (PI 3-K)/Akt signaling pathway in the balance of HSC activation and apoptosis in rat hepatic stellate cells (HSC). METHODS: An activated HSC cell line was used in this study. LY 294002, the PI 3-K/Akt signal pathway block-er was used to investigate the molecular events on apoptosis in HSC and to interpret the role of this path-way in HSC apoptosis. Immunocytochemistry, Western blot and reverse transcription polymerase chain reac-tion (RT-PCR) analysis were applied to detect the ex-pression of PI 3-K, and simultaneously phosphorylated-Akt (p-Akt) and total-Akt were determined by Western blot. The HSC apoptosis was examined by annexin-V/ propidium iodide double-labelled flow cytometry and transmission electron microscopy. RESULTS: The apoptosis rates in LY 294002 (30.82% ± 2.90%) and LY 294002 + PDGF-BB (28.16% ± 2.58%) groups were signif icantly increased compared with those of control (9.02% ± 1.81%) and PDGF-BB (4.35% ± 1.18%). PDGF-BB augmented PI 3-K and p-Akt expres-sion. LY 294002 signif icantly reduced the contents of PI 3-K and p-Akt. mRNA transcription evaluated by RT-PCR showed similar tendencies as protein expression. CONCLUSION: Inhibition of PI 3-K/Akt signaling path-way induces apoptosis in HSC. 展开更多
关键词 Hepatic fibrosis Hepatic stellate cells Phosphatidylinositol 3-kinase AKT cell apoptosis
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JNK3 involvement in nerve cell apoptosis and neurofunctional recovery after traumatic brain injury 被引量:4
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作者 Jiang Long Li Cai +3 位作者 Jintao Li Lei Zhang Haiyang Yang Tinghua Wang 《Neural Regeneration Research》 SCIE CAS CSCD 2013年第16期1491-1499,共9页
Increasing evidence has revealed that the activation of the JNK pathway participates In apoptosis o1 nerve cells and neurological function recovery after traumatic brain injury. However, which genes inI the JNK family... Increasing evidence has revealed that the activation of the JNK pathway participates In apoptosis o1 nerve cells and neurological function recovery after traumatic brain injury. However, which genes inI the JNK family are activated and their role in traumatic brain injury remain unclear. Therefore, in this study, in situ end labeling, reverse transcription-PCR and neurological function assessment were adopted to investigate the alteration of JNK1, JNK2 and JNK3 gene expression in cerebral injured rats, and their role in celt apoptosis and neurological function restoration. Results showed that JNK3 expression significantly decreased at 1 and 6 hours and 1 and 7 days post injury, but that JNK1 and JNK2 expression remained unchanged. In addition, the number of apoptotic nerve cells surrounding the injured cerebral cortex gradually reduced over time post injury. The Neurological Severity Scores gradually decreased over 1,3, 5, 14 and 28 days post injury. These findings suggested that JNK3 expression was downregulated at early stages of brain injury, which may be associated with apoptosis of nerve cells. Downregulation of JNK3 expression may promote the recovery of neurological function following traumatic brain injury. 展开更多
关键词 neural regeneration JNK1 JNK2 JNK3 traumatic brain injury TdT-mediated dUTP nick endlabeling reverse transcription-PCR cell apoptosis neurological function recovery NEUROREGENERATION
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HBx activates FasL and mediates HepG2 cell apoptosis through MLK3-MKK7-JNKs signal module 被引量:15
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作者 Ren-Xian Tang Fan-Yun Kong +4 位作者 Bao-Feng Fan Xiao-Mei Liu Hong-Juan You Peng Zhang Kui-Yang Zheng 《World Journal of Gastroenterology》 SCIE CAS CSCD 2012年第13期1485-1495,共11页
AIM: To investigate the possible mechanism by which hepatitis B virus X protein (HBx) mediates apoptosis of HepG2 cells. METHODS: HBx expression vector pcDNA3.1-X was transfected into HepG2 cells to establish an H... AIM: To investigate the possible mechanism by which hepatitis B virus X protein (HBx) mediates apoptosis of HepG2 cells. METHODS: HBx expression vector pcDNA3.1-X was transfected into HepG2 cells to establish an HBx high- expression cellular model as pcDNA3.1-X transfected group. The pcDNA3.1-X and pSilencer3.1-shHBX (HBx antagonist) were cotransfected into HepG2 cells to es- tablish an HBx low-expression model as RNAi group. Untransfected HepG2 cells and HepG2 cells transfected with negative control plasmid were used as controls. Apoptosis rate, the expression of Fas/FasL signaling pathway-related proteins and the phosphorylation lev- els of MLK3, MKK7 and JNKs, which are upstream molecules of death receptor pathways and belong to the family of mitogen-activated protein kinases (MAPKs),were measured in each group RESULTS: Compared with HepG2 cell group and RNAi group, apoptosis rate, the expression of Fas and FasL proteins, and the activation of MLK3, MKK7 and 3NKs were increased in the pcDNA3.1-X transfected group. The activation of JNKs and expression of FasL protein were inhibited in the pcDNA3.1-X transfected group when treated with a known JNK inhibitor, SP600125. When authors treated pcDNA3.1-X transfected group with K252a, a known MLK3 inhibitor, the activation of MLK3, MKK7 and 3NKs as well as expression of FasL protein was inhibited. Furthermore, cell apoptosis rate was also significantly declined in the presence of K252a in the pcDNA3.1-X transfected group. CONCLUSION: HBx can induce HepG2 cell apoptosis via a novel active MLK3-MKK7-JNKs signaling module to upregulate FasL protein expression. 展开更多
关键词 Hepatitis B virus X protein MLK3 FASL HepG2cell apoptosis
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Effects of Losartan on Cell Apoptosis and Expression of Caspase-3 and JNK Proteins in Kidney Tissue in Renal Interstitial Fibrosis Rats 被引量:3
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作者 Lu BIAN Chunhua LUO Weifeng FENG 《Medicinal Plant》 CAS 2020年第1期59-62,66,共5页
[Objectives]To investigate the effects of losartan on cell apoptosis and the expression of caspase-3 and JNK proteins in kidney tissue in the adenine-induced renal fibrosis rats.[Methods]Thirty Wistar rats were random... [Objectives]To investigate the effects of losartan on cell apoptosis and the expression of caspase-3 and JNK proteins in kidney tissue in the adenine-induced renal fibrosis rats.[Methods]Thirty Wistar rats were randomly divided into three groups:control group(n=10),model group(n=10)and losartan group(n=10).The rats in the control group received saline,while those in the model group and losartan group both received adenine by gavage,for 21 d.After the renal interstitial fibrosis model was established,the rats in the losartan group were treated with losartan[10 mg/(kg·d)],while the rats in the control group and the model group rats were administered with the same amount of saline.The course of treatment was 30 d.Finally,the renal function,blood urea nitrogen(BUN),serum creatinine(Scr),creatinine clearance rate(Ccr)and the pathological morphology of the rats were detected.The apoptosis of renal tubular epithelial cells was tested by TUNEL.The caspase-3 and JNK protein expression was tested by Western blotting.[Results]After administering adenine for 21 d,the BUN,24 MTP and kidney/body weight in the model group were increased,significantly higher than the control group(P<0.01),and the Ccr was remarkably decreased(P<0.01),signifying that the renal interstitial fibrosis model was successfully built.After treating with losartan for 30 d,the Scr,BUN,and 24 MTP were significantly decreased(P<0.01),and the Ccr was significantly increased in the losartan group(P<0.01).In addition,in comparison to the model group,renal tubular epithelial apoptosis was decreased and caspase-3 and JNK expression was downregulated in the losartan group(P<0.05).[Conclusions]Losartan can reduce the adenine-induced elevation of Scr,BUN and 24 hMPT,increase Ccr,improve general condition of renal interstitial fibrosis in rats and ameliorate the progression of chronic kidney failure(CKD).The effectiveness of losartan is probably due to its ability to regulate caspase-3,JNK protein expression and attenuate renal cell apoptosis. 展开更多
关键词 LOSARTAN Renal INTERSTITIAL FIBROSIS cell apoptosis CASPASE-3 JNK
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Correlation of PI3K/Akt signaling pathway with cell apoptosis and invasion in mantle cell lymphoma 被引量:1
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作者 Ying-Juan Lu Xiao-Shen Xia 《Journal of Hainan Medical University》 2017年第16期102-105,共4页
Objective: To study the correlation of PI3K/Akt signaling pathway with cell apoptosis and invasion in mantle cell lymphoma. Methods: A total of 38 patients who were diagnosed with mantle cell lymphoma in Xijing Hospit... Objective: To study the correlation of PI3K/Akt signaling pathway with cell apoptosis and invasion in mantle cell lymphoma. Methods: A total of 38 patients who were diagnosed with mantle cell lymphoma in Xijing Hospital Affiliated to the Fourth Military Medical University between June 2014 and March 2017 were selected as the MCL group of the research, 55 patients who were diagnosed with reactive lymphoid hyperplasia in Xijing Hospital Affiliated to the Fourth Military Medical University during the same period were selected as the control group of the research, and lymph node tissue was collected to detect the protein expression of p-PI3K and p-AKT as well as the mRNA expression of apoptosis genes and invasion genes. Results: p-PI3K and p-AKT protein expression as well as SOX11, cyclinD1, TNFAIP3, XIAP, PCNA, MMP2, MMP7, MMP9 and VEGF mRNA expression in lymph node of MCL group were significantly higher than those of control group while TNFAIP3 mRNA expression was significantly lower than that of control group;SOX11, cyclinD1, XIAP, PCNA, MMP2, MMP7, MMP9 and VEGF mRNA expression in MCL lymph node with high p-PI3K expression were significantly higher than those in MCL lymph node with low p-PI3K expression while TNFAIP3 mRNA expression was significantly lower than that in MCL lymph node with low p-PI3K expression. Conclusion: The activation of PI3K/Akt signaling pathway in mantle cell lymphoma is closely related to the tumor cell apoptosis disorder and invasion enhancement. 展开更多
关键词 MANTLE cell LYMPHOMA PHOSPHATIDYLINOSITOL 3-kinase Protein KINASE B apoptosis INVASION
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Approach for mechanism of BH3 domain counterpart BH3I-2' inducing colorectal cancer cell apoptosis
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作者 FENG Wan-yu,LIU Yang,ZHANG Zhi-cheng(The First Affiliated Hospital,China Medical University,Shenyang 110001,China) 《沈阳药科大学学报》 CAS CSCD 北大核心 2008年第S1期15-15,共1页
Objective To discuss mechanism of BH3 domain counterpart BH3I-2' inducing colorectal cancer cell apoptosis.Methods Detected inhibition ratio and apoptosis of colorectal cancer cells HCT-116,which were treated by B... Objective To discuss mechanism of BH3 domain counterpart BH3I-2' inducing colorectal cancer cell apoptosis.Methods Detected inhibition ratio and apoptosis of colorectal cancer cells HCT-116,which were treated by BH3I-2',with microplate reader and flow cytometry.Results Inhibition ratio of colorectal cancer cells,which were treated by BH3I-2',could reach about 50%.Ratio of viable apoptotic cell decreased and that of non-viable apoptotic cell increased as time went.Conclusions BH3I-2' can induce colorectal cancer cell apoptosis. 展开更多
关键词 BH3I-2’ apoptosis COLORECTAL cancer cells flow CYTOMETRY
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8-hydroxy-2-(di-n-propylamino)tetralin intervenes with neural cell apoptosis following diffuse axonal injury 被引量:3
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作者 Zhenli Mao Zhenquan Song +5 位作者 Gang Li Wei Lv Xu Zhao Bin Li Xinli Feng Youli Chen 《Neural Regeneration Research》 SCIE CAS CSCD 2013年第2期133-142,共10页
Previous studies have reported a neuroprotective effect of 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) against traumatic brain injury. In accordance with the Marmarou method, rat models of diffuse axonal in... Previous studies have reported a neuroprotective effect of 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) against traumatic brain injury. In accordance with the Marmarou method, rat models of diffuse axonal injury were established. 8-OH-DPAT was intraperitoneally injected into model rats. 8-OH-DPAT treated rats maintained at constant temperature served as normal temperature controls TUNEL results revealed that neural cell swelling, brain tissue necrosis and cell apoptosis occurred around the injured tissue. Moreover, the number of Bax-, Bcl-2- and caspase-3-positive cells increased at 6 hours after diffuse axonal injury, and peaked at 24 hours. However, brain injury was attenuated, the number of apoptotic cells reduced, Bax and caspase-3 expression decreased, and Bcl-2 expression increased at 6, 12, 24, 72 and 168 hours after diffuse axonal injury in normal temperature control and in 8-OH-DPAT-intervention rats. The difference was most significant at 24 hours. All indices in 8-OH-DPAT-intervention rats were better than those in the constant temperature group. These results suggest that 8-OH-DPAT inhibits Bax and caspase-3 expression, increases Bcl-2 expression, and reduces neural cell apoptosis, resulting in neuroprotection against diffuse axonal injury. This effect is associated with a decrease in brain temperature. 展开更多
关键词 neural regeneration brain injury 8-hydroxy-2-(di-n-propylamino)tetralin diffuse axonal injury mildhypothermia cell apoptosis Bcl-2 Bax caspase-3 neuroprotection grant-supported paper photographs-containing paper neuroregeneration
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Involvement of the Wnt signaling pathway and cell apoptosis in the rat hippocampus following cerebral ischemia/reperfusion injury 被引量:2
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作者 Bin Liu Jing Tang +3 位作者 Shiying Li Yuqin Zhang Yan Li Xiaoliu Dong 《Neural Regeneration Research》 SCIE CAS CSCD 2013年第1期70-75,共6页
We investigated the role of the Wnt signaling pathway in cerebral ischemia/reperfusion injury by examining β-catenin and glycogen synthase kinase-3β protein expression in the rat hippocampal CA1 region following acu... We investigated the role of the Wnt signaling pathway in cerebral ischemia/reperfusion injury by examining β-catenin and glycogen synthase kinase-3β protein expression in the rat hippocampal CA1 region following acute cerebral ischemia/reperfusion. Our results demonstrate that cell apoptosis increases in the CA1 region following ischemia/reperfusion. In addition, β-catenin and glycogen synthase kinase-3β protein expression gradually increases, peaking at 48 hours following reperfusion. Dickkopf-1 administration, after cerebral ischemia/reperfusion injury, results in decreased cell apoptosis, and β-catenin and glycogen synthase kinase-3β expression, in the CA1 region. This suggests that β-catenin and glycogen synthase kinase-3β, both components of the Wnt signaling pathway, participate in cell apoptosis following cerebral ischemia/reperfusion injury. 展开更多
关键词 neural regeneration brain injury Oickkopf-1 Wnt signaling pathway cell apoptosis β-catenin glycogen synthase kinase-3β protein cerebral ischemia/reperfusion injury grant-supported paper NEUROREGENERATION
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Adenosine monophosphate-activated protein kinase activation enhances embryonic neural stem cell apoptosis in a mouse model of amyotrophic lateral sclerosis 被引量:3
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作者 Yanling Sui Zichun Zhao +2 位作者 Rong Liu Bin Cai Dongsheng Fan 《Neural Regeneration Research》 SCIE CAS CSCD 2014年第19期1770-1778,共9页
Alterations in embryonic neural stem cells play crucial roles in the pathogenesis of amyotrophic lateral sclerosis. We hypothesized that embryonic neural stem cells from SOD1G93A individuals might be more susceptible ... Alterations in embryonic neural stem cells play crucial roles in the pathogenesis of amyotrophic lateral sclerosis. We hypothesized that embryonic neural stem cells from SOD1G93A individuals might be more susceptible to oxidative injury, resulting in a propensity for neurodegeneration at later stages. In this study, embryonic neural stem cells obtained from human superoxide dis- mutase 1 mutant (SOD1G93A) and wild-type (SOD1wv) mouse models were exposed to H202. We assayed cell viability with mitochondrial succinic dehydrogenase colorimetric reagent, and measured cell apoptosis by flow cytometry. Moreover, we evaluated the expression of the adenos- ine monophosphate-activated protein kinase (AMPK) ct-subunit, paired box 3 (Pax3) protein, and p53 in western blot analyses. Compared with SOD1wr cells, SOD1~93A embryonic neural stem cells were more likely to undergo H202-induced apoptosis. Phosphorylation of AMPKct in SOD1G93A cells was higher than that in SOD1wr cells. Pax3 expression was inversely correlated with the phosphorylation levels of AMPKct. p53 protein levels were also correlated with AMPKct phosphorylation levels. Compound C, an inhibitor of AMPKa, attenuated the effects of H20~. These results suggest that embryonic neural stem cells from SOD1C93A mice are more susceptible to apoptosis in the presence of oxidative stress compared with those from wild-type controls, and the effects are mainly mediated by Pax3 and p53 in the AMPKa pathway. 展开更多
关键词 nerve regeneration neuroderegeneration embryonic neural stem cells adenosine mo-nophosphate-activated protein kinase a paired box 3 p53 SOD1~93A mouse amyotrophic lateralsclerosis oxidative stress hydrogen peroxide apoptosis NSFC grants neural regeneration
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miR-24-3p promotes proliferation and inhibits apoptosis of porcine granulosa cells by targeting P27
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作者 Shengjie Shi Lutong Zhang +7 位作者 Liguang Wang Huan Yuan Haowei Sun Mielie Madaniyati Chuanjiang Cai Weijun Pang Lei Gao Guiyan Chu 《Journal of Integrative Agriculture》 SCIE CAS CSCD 2024年第4期1315-1328,共14页
Ovarian follicle development is associated with the physiological functions of granulosa cells(GCs),including proliferation and apoptosis.The level of miR-24-3p in ovarian tissue of high-yielding Yorkshire×Landra... Ovarian follicle development is associated with the physiological functions of granulosa cells(GCs),including proliferation and apoptosis.The level of miR-24-3p in ovarian tissue of high-yielding Yorkshire×Landrace sows was significantly higher than that of low-yielding sows.However,the functions of miR-24-3p on GCs are unclear.In this study,using flow cytometry,5-ethynyl-2′-de-oxyuridine(EdU)staining,and cell count,we showed that miR-24-3p promoted the proliferation of GCs increasing the proportion of cells in the S phase and upregulating the expression of cell cycle genes,moreover,miR-24-3p inhibited GC apoptosis.Mechanistically,on-line prediction,bioinformatics analysis,a luciferase reporter assay,RT-qPCR,and Western blot results showed that the target gene of miR-24-3p in proliferation and apoptosis is cyclin-dependent kinase inhibitor 1B(P27/CDKN1B).Furthermore,the effect of miR-24-3p on GC proliferation and apoptosis was attenuated by P27 overexpression.These findings suggest that miR-24-3p regulates the physiological functions of GCs. 展开更多
关键词 miR-24-3p granulosa cells PROLIFERATION apoptosis
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3-Methyladenine potentiates paclitaxel-induced apoptosis and phosphorylation of cyclin-dependent kinase 1 at thr161 in nasopharyngeal carcinoma cell
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作者 XIAOQI WU YECHUAN HE +4 位作者 YEQIN YUAN XIAN TAN LIN ZHU DANLING WANG BINYUAN JIANG 《BIOCELL》 SCIE 2024年第5期861-872,共12页
Background:Nasopharyngeal carcinoma(NPC)exhibits a significant prevalence in the southern regions of China,and paclitaxel(PTX)is frequently employed as a medication for managing advanced NPC.However,drug resistance is... Background:Nasopharyngeal carcinoma(NPC)exhibits a significant prevalence in the southern regions of China,and paclitaxel(PTX)is frequently employed as a medication for managing advanced NPC.However,drug resistance is typically accompanied by a poor prognosis.Exploring the synergistic potential of combining multiple chemotherapeutic agents may represent a promising avenue for optimizing treatment efficacy.Methods:This study investigated whether 3-Methyladenine(3-MA)could potentiated the effect of PTX and its potential molecular mechanism.Samples were divided into the following categories:Negative control(NC)with the solvent dimethyl sulfoxide(DMSO,0.5%v/v),PTX(400 nM),3-MA(4 mM),and PTX(400 nM)+3-MA(4 mM).The viability of NPC cells was assessed using both the cell counting kit-8(CCK-8)assay and the colony formation assay.Microscopic observation was performed to identify morphological cell changes.Flow cytometry was used to assess cell cycle status,mitochondrial membrane potential(MMP),and apoptotic cells.Western blotting was conducted to quantify the protein expression.Results:3-MA enhanced PTX-specific inhibition of NPC cell proliferation.PTX,either alone or in combination with 3-MA,caused cell cycle halt at the G2/M phase in the majority of NPC cells,and the combination treatment of PTX with 3-MA induced a higher rate of NPC cell death compared to PTX alone.Western blotting results revealed the combination of PTX with 3-MA heightened activation of cyclin-dependent kinase 1(CDK1),a key molecule in shifting cells from mitotic arrest to apoptosis,led to a reduction in Myeloid Cell Leukemia 1(MCL-1)expression and an increase in Poly(ADP-ribose)polymerase(PARP)cleavage.Conclusion:The concurrent administration of PTX with 3-MA effectively enhances PTX’s inhibitory impact on NPC and activates the apoptosis signal regulated by CDK1. 展开更多
关键词 Nasopharyngeal carcinoma PACLITAXEL 3-Methyladenine cell cycle apoptosis
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Effect of cocaine on germ cell apoptosis in rats at different ages
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作者 Guo-Sheng Yang Wei Wang Yi-Min Wang Zhao-Dian Chen Shuo Wang Jia-Jie Fang 《Asian Journal of Andrology》 SCIE CAS CSCD 2006年第5期569-575,共7页
Aim: To investigate the effect of cocaine on apoptosis and caspase-3 activity in germ cells in male rats at different ages. Methods: Cocaine hydrochloride was given (15 mg/kg body weight s.c.) to male Sprague-Dawl... Aim: To investigate the effect of cocaine on apoptosis and caspase-3 activity in germ cells in male rats at different ages. Methods: Cocaine hydrochloride was given (15 mg/kg body weight s.c.) to male Sprague-Dawley rats of 3 weeks (n = 8), 6 weeks (n = 8) and 12 weeks (n = 8) of age, daily for 28 days. The serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), testosterone (T) and estrogen (E2) were assayed, and the DNA fragmentation of germ cells was determined by gel eletronphoresis. The cell cycle, apoptosis and caspase-3 activity of germ cells were tested by flow cytometry. Results: After the 28-day cocaine treatment, testes weight of the 3-week-old rats, the testes and body weights of the 6-week-old rats were decreased significantly compared to those of their corresponding controls (P 〈 0.05). The serum level of T was decreased significantly in the 3-week-old and 6-week-old rats, and the serum level of PRL was also decreased significantly in 12-week-old rats compared to the controls (P 〈 0.05), In all the three cocaine-treated groups, the isolated DNA displayed a clear ladder pattern, especially in the 6-week old rats. The number of apoptosic germ cells increased significantly in 3- and 6- week-old rats treated with cocaine (P 〈 0.05). The caspase-3 activity in all three groups increased significantly compared to the controls (P 〈 0.05), especially in the 6-week-old rats. Conclusion: Cocaine exposure for 28 days leads to significant damage to male gonad and apoptosis elevation in testes of rats of different ages, especially in those of 6 weeks of age. The increase in caspase-3 activity might be a key pathway related to the early stage of apoptosis as the mechanism of cocaine-induced germ cell loss. 展开更多
关键词 COCAINE TESTIS apoptosis CASPASE-3 germ cell
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Mechanism of stilbene glycosides on apoptosis of SH-SY5Y cells via regulating PI3K/AKT signaling pathway
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作者 KANG Bi-qian LI Yue +8 位作者 HE Xiao-xuan XIAO Zhen HU Rui LUO Chen-liang QIAO Ming-yu WU Gui-you LI Zhen-zhong ZHU Xiao-ying HUANG Zhong-shi 《Journal of Hainan Medical University》 CAS 2024年第1期8-14,共7页
Objective:To investigate the effects of stilbene glycoside(TSG)on okadaic acid-induced apoptosis in human neuroblastoma cells(SH-SY5Y)via the PI3K/AKT pathway.Methods:The optimal concentration of OA was screened by CC... Objective:To investigate the effects of stilbene glycoside(TSG)on okadaic acid-induced apoptosis in human neuroblastoma cells(SH-SY5Y)via the PI3K/AKT pathway.Methods:The optimal concentration of OA was screened by CCK-8 assay,and SH-SY5Y cells were divided into control group,model group,TSG group,LY294002 group and LY294002+TSG group.The proliferation and apoptosis in each group were detected by CCK-8 and TUNEL assays;Western blotting method and real-time fluorescence quantitative polymerase chain reaction was used to detect the expression of PI3K,P-PI3K(Y607),AKT,P-AKT(Ser473),Bcl-2 and Bax proteins.The relative protein expression was represented by P-PI3K(Y607)/PI3K,P-AKT(Ser473)/AKT and Bcl-2/Bax gray ratio.Results:CCK-8 screened the optimal concentration of OA as 40 nmol/L.Compared with the control group,the model group increased relative cell viability,decreased apoptosis rate,the pathway and apoptotic proteins expression levels of P-PI3K(Y607)/PI3K,P-AKT(Ser473)/AKT and Bcl-2/Bax were decreased,and the mRNA expression levels of PI3K,AKT and Bcl-2 were decreased.Bax mRNA expression level increased(P<0.05);Compared with model group,TSG group increased relative cell viability,decreased apoptosis rate,increased protein expression levels of P-PI3K(Y607)/PI3K,P-AKT(Ser473)/AKT,Bcl-2/Bax,and increased mRNA expression levels of PI3K,AKT,and Bcl-2.Bax mRNA expression decreased(P<0.05),LY294002 group decreased relative cell viability,increased apoptosis rate,P-PI3K(Y607)/PI3K protein expression levels were significantly decreased(P<0.05),P-AKT(Ser473)/AKT and Bcl-2/Bax protein expression levels were significantly decreased,but there was no statistical significance,PI3K,AKT and Bcl-2 mRNA expression levels were decreased,and Bax mRNA expression levels were increased(all P<0.05);Compared with LY294002 group,LY294002+TSG group increased relative cell viability,decreased apoptosis rate,and the protein expression levels of P-PI3K(Y607)/PI3K,P-AKT(Ser473)/AKT and Bcl-2/Bax were increased.The mRNA expression levels of PI3K,AKT,Bcl-2 were increased,Bax was decreased(all P<0.05).Conclusion:Stilbene glycoside may alleviate okadaic acid-induced apoptosis in SH-SY5Y cells by interfering with the PI3K/AKT signaling pathway,which in turn regulates the expression of apoptotic factors such as Bcl-2 and Bax. 展开更多
关键词 2 3 5 4'-tetrahydroxystilbene 2-O-glucopyranoside Alzheimer disease LY294002 Phosphatidylinositol 3-kinase(PI3K)/protein kinase B(AKT) cell proliferation apoptosis
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Dihydromyricetin Alleviates H9C2 Cell Apoptosis and Autophagy by Regulating CircHIPK3 Expression and PI3K/AKT/mTOR Pathway 被引量:2
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作者 ZHANG Zhi-ying LIU Chao +5 位作者 WANG Peng-xiang HAN Yi-wei ZHANG Yi-wen HAO Mei-li SONG Zi-xu ZHANG Xiao-ying 《Chinese Journal of Integrative Medicine》 SCIE CAS CSCD 2023年第5期434-440,共7页
Objective: To investigate the effect and potential mechanism of dihydromyricetin(Dmy) on H9C2 cell proliferation, apoptosis, and autophagy. Methods: H9C2 cells were randomly divided into 7 groups, namely control, mode... Objective: To investigate the effect and potential mechanism of dihydromyricetin(Dmy) on H9C2 cell proliferation, apoptosis, and autophagy. Methods: H9C2 cells were randomly divided into 7 groups, namely control, model, EV(empty p CDH-CMV-MCS-EF1-Cop GFP-T2A-Puro vector), IV(circHIPK3 interference), Dmy(50 μmol/L), Dmy+IV, and Dmy+EV groups. Cell proliferation and apoptosis were detected by cell counting kit-8 assay and flow cytometry, respectivley. Western blot was used to evaluate the levels of light chain 3 Ⅱ/Ⅰ(LC3Ⅱ/Ⅰ), phospho-phosphoinositide 3-kinase(p-PI3K), protein kinase B(p-AKT), and phospho-mammalian target of rapamycin(p-mTOR). The level of circHIPK3 was determined using reverse transcriptase polymerase chain reaction. Electron microscopy was used to observe autophagosomes in H9C2 cells. Results: Compared to H9C2 cells, the expression of circHIPK in H9C2 hypoxia model cells increased significantly(P<0.05). Compared to the control group, the cell apoptosis and autophagosomes increased, cell proliferation rate decreased significantly, and the expression of LC3Ⅱ/Ⅰ significantly increased(all P<0.05). Compared to the model group, the rate of apoptosis and autophagosomes in IV, Dmy, and Dmy+IV group decreased, the cell proliferation rate increased, and the expression of LC3Ⅱ/Ⅰ decreased significantly(all P<0.05). Compared to the control group, the expressions of p-PI3K, p-AKT, and p-mTOR in the model group significantly reduced(P<0.05), whereas after treatment with Dmy and sh-circHIPK3, the above situation was reversed(P<0.05). Conclusion: Dmy plays a protective role in H9C2 cells by inhibiting circHIPK expression and cell apoptosis and autophagy, and the mechanism may be related to PI3K/AKT/mTOR pathway. 展开更多
关键词 DIHYDROMYRICETIN circHIPK AUTOPHAGY cell apoptosis PI3K/AKT/MTOR
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Dioscin from Polygonatum sibiricum induces apoptosis and autophagy in Ishikawa human endometrial cancer cell and in vivo
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作者 Xiaoli Li Runhui Ma +4 位作者 Zhijing Ni Wei Wang Kiran Thakur Jianguo Zhang Zhaojun Wei 《Food Science and Human Wellness》 SCIE CAS CSCD 2024年第5期2601-2616,共16页
With an aim to comprehend the precise regulatory mechanism of dioscin against endometrial carcinoma(EC), we firstly extracted the components from Polygonatum sibiricum followed by identification and structural charact... With an aim to comprehend the precise regulatory mechanism of dioscin against endometrial carcinoma(EC), we firstly extracted the components from Polygonatum sibiricum followed by identification and structural characterization. The anti-EC activity of dioscin was initially determined based on the inhibition of Ishikawa cell proliferation and tumor growth. The high-throughput sequencing data indicated that dioscin not only promoted apoptosis, including decrease of poly ADP-ribose polymerase(PARP) and B-cell lymphoma-2(Bcl-2) and increase of c-PARP and Bcl-2-associcated agonist of cell death(Bad), but also induced autophagy, including increase of autophagic lysosomes and LC3Ⅱ/LC3Ⅰ ratio. Mechanistic exploration suggested that dioscin induced autophagy and apoptosis through inhibition of PI3K/AKT/mTOR signaling pathway. Besides, the dioscin-regulated p53 pathway was mainly involved in autophagy induction. Furthermore, inhibition of Ishikawa cell autophagy was linked to dioscin-induced apoptosis. Our data suggest the immense potential of dioscin for the development of functional food for EC and related medical application. 展开更多
关键词 DIOSCIN Ishikawa cell apoptosis AUTOPHAGY PI3K/AKT p53
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Antitumor Effect of Apcin on Endometrial Carcinoma via p21-Mediated Cell Cycle Arrest and Apoptosis
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作者 Ke NI Zi-li LI +1 位作者 Zhi-yong HU Li HONG 《Current Medical Science》 SCIE CAS 2024年第3期623-632,共10页
Objective Endometrial carcinoma(EC)is a prevalent gynecological malignancy characterized by increasing incidence and mortality rates.This underscores the critical need for novel therapeutic targets.One such potential ... Objective Endometrial carcinoma(EC)is a prevalent gynecological malignancy characterized by increasing incidence and mortality rates.This underscores the critical need for novel therapeutic targets.One such potential target is cell division cycle 20(CDC20),which has been implicated in oncogenesis.This study investigated the effect of the CDC20 inhibitor Apcin on EC and elucidated the underlying mechanism involved.Methods The effects of Apcin on EC cell proliferation,apoptosis,and the cell cycle were evaluated using CCK8 assays and flow cytometry.RNA sequencing(RNA-seq)was subsequently conducted to explore the underlying molecular mechanism,and Western blotting and coimmunoprecipitation were subsequently performed to validate the results.Animal studies were performed to evaluate the antitumor effects in vivo.Bioinformatics analysis was also conducted to identify CDC20 as a potential therapeutic target in EC.Results Treatment with Apcin inhibited proliferation and induced apoptosis in EC cells,resulting in cell cycle arrest.Pathways associated with apoptosis and the cell cycle were activated following treatment with Apcin.Notably,Apcin treatment led to the upregulation of the cell cycle regulator p21,which was verified to interact with CDC20 and consequently decrease the expression of downstream cyclins in EC cells.In vivo experiments confirmed that Apcin treatment significantly impeded tumor growth.Higher CDC20 expression was observed in EC tissue than in nonmalignant tissue,and increased CDC20 expression in EC patients was associated with shorter overall survival and progress free interval.Conclusion CDC20 is a novel molecular target in EC,and Apcin could be developed as a candidate antitumor drug for EC treatment. 展开更多
关键词 endometrial carcinoma CDC20 apoptosis cell cycle arrest P21 BBC3
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Demethylation of miR-34a upregulates expression of membrane palmitoylated proteins and promotes the apoptosis of liver cancer cells 被引量:5
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作者 Fu-Yong Li Ting-Yong Fan +1 位作者 Hao Zhang Yu-Min Sun 《World Journal of Gastroenterology》 SCIE CAS 2021年第6期470-486,共17页
BACKGROUND Liver cancer is a common cancer and the main cause of cancer-related deaths worldwide.Liver cancer is the sixth most common cancer in the world.Although miR-34a and palmitoyl membrane palmitoylated protein(... BACKGROUND Liver cancer is a common cancer and the main cause of cancer-related deaths worldwide.Liver cancer is the sixth most common cancer in the world.Although miR-34a and palmitoyl membrane palmitoylated protein(MPP2)are reportedly involved in various cell processes,their precise roles in liver cancer are still unclear.AIM To investigate the expression of micro RNA 34a(miR-34a),methylation of the miR-34a promoter and the expression of MPP2 in liver cancer cells and their related mechanisms.METHODS Together,78 cases of liver cancer tissues and 78 cases of adjacent tissues were collected.The methylation degree of miR-34a promoter in liver cancer/paracancerous tissue and liver cancer cells/normal liver cells,and the expression levels of miR-34a and MPP2 in the above samples were detected.Demethylation of liver cancer cells or transfection of liver cancer cells with miR-34a mimetic was performed.The MPP2 overexpression vector was used to transfect liver cancer cells,and the changes in proliferation,invasion,apoptosis,migration,and other biological functions of liver cancer cells after the above interventions were observed.Double luciferase reporter genes were used to detect the targeting relationship between miR-34a and MPP2.RESULTS Clinical samples showed that the expression levels of miR-34a and MPP2 in liver cancer tissues were lower than those in the normal tissues.The methylation degree of miR-34a promoter region in liver cancer cells was higher than that in normal liver cells.After miR-34a demethylation/mimetic transfection/MPP2 overexpression,the apoptosis of liver cancer cells was increased;the proliferation,invasion and migration capabilities were decreased;the expression levels of caspase 3,caspase 9,E-cadherin,and B-cell lymphoma 2(Bcl-2)-associated X protein were increased;and the expression levels of Bcl-2,N-cadherin,andβ-catenin were decreased.Double luciferase reporter genes confirmed that MPP2 is targeted by miR-34a.Rescue experiments showed that small interfering MPP2 could counteract the promoting effect of miR-34a demethylation on apoptosis and the inhibitory effect on cell proliferation,invasion,and migration.CONCLUSION miR-34a demethylation upregulates the expression level of MPP2 in liver cancer cells and promotes the apoptosis of liver cancer cells.miR-34a demethylation is a potential method for liver cancer treatment. 展开更多
关键词 Liver cancer MIR-34A Membrane palmitoylated proteins Methylation cell apoptosis Caspase 3
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Japanese Encephalitis Virus NS2B-3 Protein Complex Promotes Cell Apoptosis and Viral Particle Release by Down-Regulating the Expression of AXL 被引量:1
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作者 Shengda Xie Zhenjie Liang +4 位作者 Xingmiao Yang Junhui Pan Du Yu Tongtong Li Ruibing Cao 《Virologica Sinica》 SCIE CAS CSCD 2021年第6期1503-1519,共17页
Japanese encephalitis virus(JEV) is a flavivirus transmitted by mosquitoes that causes severe encephalitis in humans and animals. It has been suggested that AXL, a transmembrane protein, can promote the replication of... Japanese encephalitis virus(JEV) is a flavivirus transmitted by mosquitoes that causes severe encephalitis in humans and animals. It has been suggested that AXL, a transmembrane protein, can promote the replication of various flaviviruses,such as dengue(DENV), Zika(ZIKV), and West Nile(WNV) viruses. However, the effect of AXL on JEV infection has not yet been determined. In the present study, we demonstrate that AXL is down-regulated after JEV infection in the late stage. JEV NS2B-3 protein specifically interacted with AXL, and promoted AXL degradation through the ubiquitin–proteasome pathway. AXL-degradation increased cell apoptosis by disrupting phosphatidylinositol 3-kinase(PI3 K)/Akt signal transduction. In addition, the degradation of AXL promoted JEV release to supernatant, whereas the virus in the cell lysates decreased. The supplementation of AXL ligand Gas6 inhibited the JEV-mediated degradation of AXL. Altogether,we discover a new function of NS2B-3 during the process of JEV replication, and provide a new insight into the interactions between JEV and cell hosts. 展开更多
关键词 Japanese encephalitis virus(JEV) AXL NS2B-3 cell apoptosis Virus release
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