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血必净注射液通过PTEN/PI3K/Akt/mTOR信号通路对大鼠肺缺血再灌注损伤的影响
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作者 杨淼 鄢见勇 +2 位作者 郑坤 邹平洋 华妤 《医学理论与实践》 2024年第13期2161-2164,共4页
目的:探讨血必净注射液对肺缺血再灌注损伤的保护作用及其相关机制。方法:选择18只健康成年雄性大鼠,随机分为正常对照组(Sham组)、肺缺血再灌注组(LIR组)、血必净注射液组(XBJ组),采用开胸夹闭左肺门构建肺缺血再灌注损伤大鼠模型,苏... 目的:探讨血必净注射液对肺缺血再灌注损伤的保护作用及其相关机制。方法:选择18只健康成年雄性大鼠,随机分为正常对照组(Sham组)、肺缺血再灌注组(LIR组)、血必净注射液组(XBJ组),采用开胸夹闭左肺门构建肺缺血再灌注损伤大鼠模型,苏木素—伊红染色观察各组大鼠肺组织病理学改变,检测各组大鼠肺组织湿/干重比(W/D)及肺组织炎症因子IL-1β、TNF-α水平,Western Blot检测各组肺组织PTEN、PI3K、Akt、mTOR、LC3-Ⅰ、LC3-Ⅱ、p62蛋白表达,qRT-PCR检测各组肺组织PTEN、PI3K、Akt、mTOR mRNA表达。结果:血必净注射液可显著减轻肺缺血再灌注大鼠肺组织损伤,降低缺血再灌注大鼠肺组织W/D及IL-1β、TNF-α含量(P<0.05)。与Sham组相比,LIR组、XBJ组PTEN、PI3K、Akt、mTOR、LC3-Ⅰ、LC3-Ⅱ、p62表达均升高(P<0.05);与LIR组相比,XBJ组PTEN、LC3-Ⅰ、LC3-Ⅱ、p62表达降低(P<0.05),PI3K、Akt、mTOR表达升高(P<0.05)。与Sham组相比,LIR组、XBJ组PTEN、PI3K、Akt、mTOR mRNA表达升高(P<0.05);与LIR组相比,XBJ组PTEN mRNA表达降低(P<0.05),PI3K、Akt、mTOR mRNA表达升高(P<0.05)。结论:血必净注射液可能通过抑制PTEN,激活PI3K/Akt/mTOR信号通路抑制肺缺血再灌注损伤自噬水平,从而改善肺缺血再灌注损伤,达到保护肺组织的作用。 展开更多
关键词 血必净注射液 pten/PI3K/Akt/mtor信号通路 肺缺血再灌注损伤
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Spi1 regulates the microglial/macrophage inflammatory response via the PI3K/AKT/mTOR signaling pathway after intracerebral hemorrhage
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作者 Guoqiang Zhang Jianan Lu +7 位作者 Jingwei Zheng Shuhao Mei Huaming Li Xiaotao Zhang An Ping Shiqi Gao Yuanjian Fang Jun Yu 《Neural Regeneration Research》 SCIE CAS CSCD 2024年第1期161-170,共10页
Preclinical and clinical studies have shown that microglia and macrophages participate in a multiphasic brain damage repair process following intracerebral hemorrhage.The E26 transformation-specific sequence-related t... Preclinical and clinical studies have shown that microglia and macrophages participate in a multiphasic brain damage repair process following intracerebral hemorrhage.The E26 transformation-specific sequence-related transcription factor Spi1 regulates microglial/macrophage commitment and maturation.However,the effect of Spi1 on intracerebral hemorrhage remains unclear.In this study,we found that Spi1 may regulate recovery from the neuroinflammation and neurofunctional damage caused by intracerebral hemorrhage by modulating the microglial/macrophage transcriptome.We showed that high Spi1expression in microglia/macrophages after intracerebral hemorrhage is associated with the activation of many pathways that promote phagocytosis,glycolysis,and autophagy,as well as debris clearance and sustained remyelination.Notably,microglia with higher levels of Soil expression were chara cterized by activation of pathways associated with a variety of hemorrhage-related cellular processes,such as complement activation,angiogenesis,and coagulation.In conclusion,our results suggest that Spi1 plays a vital role in the microglial/macrophage inflammatory response following intracerebral hemorrhage.This new insight into the regulation of Spi1 and its target genes may advance our understanding of neuroinflammation in intracerebral hemorrhage and provide therapeutic targets for patients with intracerebral hemorrhage. 展开更多
关键词 intracerebral hemorrhage MACROPHAGE microglia neuroinflammation PHAGOCYTOSIS PI3K/AKT/mtor signaling pathway Spi1 TRANSCRIPTOMICS
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Downregulation of Serum PTEN Expression in Mercury-Exposed Population and PI3K/AKT Pathway-Induced Inflammation
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作者 MEI Peng DING En Min +6 位作者 YIN Hao Yang DING Xue Xue WANG Huan WANG Jian Feng HAN Lei ZHANG Heng Dong ZHU Bao Li 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2024年第4期354-366,共13页
Objective This study investigated the impact of occupational mercury(Hg) exposure on human gene transcription and expression, and its potential biological mechanisms.Methods Differentially expressed genes related to H... Objective This study investigated the impact of occupational mercury(Hg) exposure on human gene transcription and expression, and its potential biological mechanisms.Methods Differentially expressed genes related to Hg exposure were identified and validated using gene expression microarray analysis and extended validation. Hg-exposed cell models and PTEN lowexpression models were established in vitro using 293T cells. PTEN gene expression was assessed using qRT-PCR, and Western blotting was used to measure PTEN, AKT, and PI3K protein levels. IL-6 expression was determined by ELISA.Results Combined findings from gene expression microarray analysis, bioinformatics, and population expansion validation indicated significant downregulation of the PTEN gene in the high-concentration Hg exposure group. In the Hg-exposed cell model(25 and 10 μmol/L), a significant decrease in PTEN expression was observed, accompanied by a significant increase in PI3K, AKT, and IL-6 expression.Similarly, a low-expression cell model demonstrated that PTEN gene knockdown led to a significant decrease in PTEN protein expression and a substantial increase in PI3K, AKT, and IL-6 levels.Conclusion This is the first study to report that Hg exposure downregulates the PTEN gene, activates the PI3K/AKT regulatory pathway, and increases the expression of inflammatory factors, ultimately resulting in kidney inflammation. 展开更多
关键词 pten Occupational mercury exposure Occupational health PI3K/AKT pathway 293T cell IL-6
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Alleviatory effect of isoquercetin on benign prostatic hyperplasia via IGF-1/PI3K/Akt/mTOR pathway
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作者 Young-Jin Choi Meiqi Fan +2 位作者 Nishala Erandi Wedamulla Yujiao Tang Eun-Kyung Kim 《Food Science and Human Wellness》 SCIE CSCD 2024年第3期1698-1710,共13页
We evaluated the effect of isoquercetin(quercetin-O-3-glucoside-quercetin,IQ)as a functional component of Abeliophyllum disistichum Nakai ethanol extract(ADLE)on prostate cell proliferation and apoptosis and its effec... We evaluated the effect of isoquercetin(quercetin-O-3-glucoside-quercetin,IQ)as a functional component of Abeliophyllum disistichum Nakai ethanol extract(ADLE)on prostate cell proliferation and apoptosis and its effects on the IGF-1/PI3K/Akt/mTOR pathway in benign prostatic hyperplasia(BPH).Metabolites in ADLE were analyzed using UHPLC-qTOF-MS and HPLC.IQ was orally administered(1 or 10 mg/kg)to a testosterone propionate-induced BPH rat model,and its effects on the prostate weight were evaluated.The effect of IQ on androgen receptor(AR)signaling was analyzed in LNCaP cells.Whether IGF-1 and IQ affect the IGF-1/PI3K/Akt/mTOR pathway in BPH-1 cells was also examined.The metabolites in ADLE were identified and quantified,which confirmed that ADLE contained abundant IQ(20.88 mg/g).IQ significantly reduced the prostate size in a concentration-dependent manner in a BPH rat model,and significantly decreased the expression of AR signaling factors in the rat prostate tissue and LNCaP cells in a concentration-dependent manner.IQ also inhibited the PI3K/AKT/mTOR pathway activated by IGF-1 treatment in BPH-1 cells.In BPH-1 cells,IQ led to G0/G1 arrest and suppressed the expression of proliferation factors while inducing apoptosis.Thus,IQ shows potential for use as a pharmaceutical and nutraceutical for BPH. 展开更多
关键词 ISOQUERCETIN Benign prostatic hyperplasia Androgen receptor signaling PI3K/Akt/mtor pathway
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加味芪黄饮改善糖尿病肾病的PTEN/PI3K/Akt/mTOR通路机制研究
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作者 吴立友 毛凯凤 +3 位作者 谢丹丹 王玉洁 李季 黄浩东 《深圳中西医结合杂志》 2024年第7期4-8,I0002,I0003,共7页
目的:研究加味芪黄饮通过PTEN/磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(Akt)/哺乳动物雷帕霉素靶标(mTOR)通路改善糖尿病肾病(DN)的作用机制。方法:Sprague-Dawle(SD)大鼠利用高脂饲料饲养联合腹腔注射链脲佐菌素(STZ)建立DN模型,采用完全随... 目的:研究加味芪黄饮通过PTEN/磷脂酰肌醇3激酶(PI3K)/蛋白激酶B(Akt)/哺乳动物雷帕霉素靶标(mTOR)通路改善糖尿病肾病(DN)的作用机制。方法:Sprague-Dawle(SD)大鼠利用高脂饲料饲养联合腹腔注射链脲佐菌素(STZ)建立DN模型,采用完全随机法分为模型组、加味芪黄饮低剂量组、中剂量组、高剂量组及氯沙坦组。各10只。根据临床用量换算,设定加味芪黄饮低剂量组、中剂量组、高剂量组[生药含量:200、400、800 mg·kg^(-1)·d^(-1)],空白组及模型组予0.9%氯化钠注射液灌胃。8周后取材,检测DN大鼠24 h尿蛋白、血肌酐(SCr)、血尿素氮水平(BUN),苏木精-伊红(HE)染色观察肾脏病理变化,免疫组化检测肾组织中PTEN、PI3K、Akt和mTOR等蛋白表达。结果:与空白组相比,模型组大鼠24 h尿蛋白、SCr、BUN水平显著升高(P<0.0001);加味芪黄饮干预后肾功能指标相比于模型组有所降低(P<0.001),免疫组化结果提示:模型组PTEN表达降低,PI3K、Akt、mTOR表达升高(P<0.01);加味芪黄饮干预后,PTEN表达量上升,PI3K、Akt及mTOR表达量下降,相比模型组差异均具有统计学意义(P<0.05)。加味芪黄饮高剂量组与氯沙坦组疗效差异无统计学意义(P>0.05)。结论:加味芪黄饮可能通过PTEN/PI3K/Akt/mTOR通路延缓DN发展。 展开更多
关键词 糖尿病肾病 加味芪黄饮 pten/PI3K/Akt/mtor
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阿伐他汀通过PTEN/mTOR信号调节糖酵解代谢逆转白血病耐药的作用及机制
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作者 刘苗 周攀 《中国实验血液学杂志》 CAS CSCD 北大核心 2023年第1期38-44,共7页
目的:探讨阿伐他汀对耐阿霉素人急性早幼粒白血病细胞系HL-60/ADM糖酵解代谢的影响及作用机制。方法:取对数生长期耐阿霉素白血病细胞HL-60/ADM,给予不同浓度阿伐他汀处理后,采用CCK-8法测定细胞增殖活性,流式细胞术检测细胞凋亡,葡萄... 目的:探讨阿伐他汀对耐阿霉素人急性早幼粒白血病细胞系HL-60/ADM糖酵解代谢的影响及作用机制。方法:取对数生长期耐阿霉素白血病细胞HL-60/ADM,给予不同浓度阿伐他汀处理后,采用CCK-8法测定细胞增殖活性,流式细胞术检测细胞凋亡,葡萄糖消耗实验检测白血病细胞糖酵解活性,Western blot方法检测PTEN、p-m TOR、PKM2、HK2、P-gp、MRP1蛋白的表达;将PTEN-si RNA转染至HL-60/ADM细胞后,进一步采用上述方法检测PTEN低表达对阿伐他汀调节HL-60/ADM细胞凋亡及糖酵解代谢的影响。结果:CCK-8结果显示,阿伐他汀呈浓度依赖性和时间依赖性抑制HL-60/ADM细胞增殖(r=0.872,r=0.936),10μmol/L阿伐他汀干预24 h后HL-60/ADM细胞增殖活性下降最明显,增殖活性降至(32.3±2.18)%。流式细胞术结果显示,阿伐他汀诱导HL-60/ADM细胞凋亡,该作用呈浓度依赖性(r=0.796),10μmol/L阿伐他汀对HL-60/ADM细胞的诱导凋亡作用最强,细胞凋亡率达到(48.78±2.95)%。葡萄糖消耗实验结果表明阿伐他汀明显抑制HL-60/ADM细胞糖酵解活性,该作用呈浓度依赖性和时间依赖性(r=0.915,r=0.748),10μmol/L阿伐他汀干预24 h后对糖酵解活性的抑制作用最强,相对葡萄糖消耗量降至(46.53±1.71)%。Western blot结果显示,给予阿伐他汀干预24 h后,p-m TOR、PKM2、HK2、P-gp、MRP1蛋白表达呈浓度依赖性降低(r=0.737,r=0.695,r=0.829,r=0.781,r=0.632),而PTEN蛋白表达呈浓度依赖性升高(r=0.531)。进一步将PTEN-si RNA转染HL-60/ADM细胞,结果显示,低表达PTEN减弱了阿伐他汀对细胞凋亡的促进作用以及对糖酵解代谢和多药耐药的抑制作用。结论:阿伐他汀能抑制白血病耐药株HL-60/ADM细胞增殖,诱导细胞凋亡,抑制糖酵解代谢,推测机制可能是通过上调PTEN表达,抑制m TOR激活,下调PKM2和HK2糖酵解代谢基因表达,从而逆转耐药。 展开更多
关键词 阿伐他汀 白血病耐药 pten/mtor通路 糖酵解
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How is the AKT/mTOR pathway involved in cell migration and invasion? 被引量:1
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作者 JINGYAO XU SHUANGLI HAO +2 位作者 KAIYUE HAN WANXI YANG HONG DENG 《BIOCELL》 SCIE 2023年第4期773-788,共16页
As a pathway that plays a role in nutrient absorption,anabolic response,cell growth and survival,the important role of AKT/mTOR in tumorigenesis has also come to light.For cancer patients,most deaths are caused by the... As a pathway that plays a role in nutrient absorption,anabolic response,cell growth and survival,the important role of AKT/mTOR in tumorigenesis has also come to light.For cancer patients,most deaths are caused by the growth of metastatic tumors outside the primary focus.Therefore,migration and invasion in the late stage of tumor progression are the main unresolved issues in the study of tumor pathogenesis,and AKT/mTOR has been found to participate in the migration and invasion of cancer cells,which means that the study of this pathway may contribute to a solution for the problem.Because of its extensive and complex functions in the organism,this pathway can be regulated by a variety of different signals in the body,and then realize its function through different downstream signal molecules.This article reviews the proteins that can indirectly affect this pathway by regulating the common upstream signaling molecules of this pathway,and the proteins that can directly affect the level of phosphorylation of AKT/mTOR in cancer cells.We also review the proteins that can co-regulate this pathway and its downstream pathways.Through this study,we hope to gain a deeper understanding of the regulatory mechanism of the AKT/mTOR pathway in cancer cells,in hopes of finding effective and harmless cancer treatment targets in the future. 展开更多
关键词 AKT/mtor Migration and invasion Cancer cell Signal pathway REGULATION
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LAMC2 regulates proliferation, migration, and invasion mediated by the Pl3K/AKT/mTOR pathway in oral 被引量:1
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作者 FAYU SHAN LANLAN LIANG +7 位作者 CHONG FENG HONGBAO XU ZIROU WANG WEILI LIU LINGLING PU ZHAOLI CHEN GANG CHEN XINXING WANG 《Oncology Research》 SCIE 2023年第4期481-493,共13页
Background:Oral squamous cell carcinoma(OSCC)is a common malignant tumor.Recently,Laminin Gamma 2(LAMC2)has been shown to be abnormally expressed in OSCC;however,how LAMC2 signaling contributes to the occurrence and d... Background:Oral squamous cell carcinoma(OSCC)is a common malignant tumor.Recently,Laminin Gamma 2(LAMC2)has been shown to be abnormally expressed in OSCC;however,how LAMC2 signaling contributes to the occurrence and development of OSCC and the role of autophagy in OSCC has not been fully explored.This study aimed to analyze the role and mechanism of LAMC2 signaling in OSCC and the involvement of autophagy in OSCC.Methods:To explore the mechanism by which LAMC2 is highly expressed in OSCC,we used small interfering RNA(siRNA)to knock down LAMC2 to further observe the changes in the signaling pathway.Furthermore,we used cell proliferation assays,Transwell invasion assays,and wound-healing assays to observe the changes in OSCC proliferation,invasion,and metastasis.RFP-LC3 was used to detect the level of autophagy intensity.A cell line-derived xenograft(CDX)model was used to detect the effect of LAMC2 on tumor growth in vivo.Results:This study found that the level of autophagy was correlated with the biological behavior of OSCC.The downregulation of LAMC2 activated autophagy and inhibited OSCC proliferation,invasion,and metastasis via inhibiting the PI3K/AKT/mTOR pathway.Moreover,autophagy has a dual effect on OSCC,and the synergistic downregulation of LAMC2 and autophagy can inhibit OSCC metastasis,invasion,and proliferation via the PI3K/AKT/mTOR pathway.Conclusions:LAMC2 interacts with autophagy to regulate OSCC metastasis,invasion,and proliferation via the PI3K/AKT/mTOR pathway.LAMC2 down-regulation can synergistically modulate autophagy to inhibit OSCC migration,invasion,and proliferation. 展开更多
关键词 LAMC2 OSCC AUTOPHAGY PI3K/AKT/mtor pathway 3-Methyladenine RAPAMYCIN
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黄芩苷通过miR-23a-3p/PTEN/PI3K/AKT/mTOR抑制痛风性关节炎成纤维样滑膜细胞炎症反应机制探究
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作者 张先恒 刘健 +2 位作者 孙艳秋 丁香 陈晓露 《山西中医药大学学报》 2023年第10期1151-1160,共10页
目的:探究黄芩苷(baicalin)通过微RNA-23a-3p/磷酸酶与紧张素同源物/磷脂酰肌醇-3-激酶/蛋白激酶B/哺乳动物雷帕霉素靶蛋白(miR-23a-3p/PTEN/PI3K/AKT/mTOR)抑制痛风性关节炎(GA)成纤维样滑膜细胞(FLS)炎症反应的机制。方法:提取GA患者... 目的:探究黄芩苷(baicalin)通过微RNA-23a-3p/磷酸酶与紧张素同源物/磷脂酰肌醇-3-激酶/蛋白激酶B/哺乳动物雷帕霉素靶蛋白(miR-23a-3p/PTEN/PI3K/AKT/mTOR)抑制痛风性关节炎(GA)成纤维样滑膜细胞(FLS)炎症反应的机制。方法:提取GA患者和正常人外周血辅助性T淋巴细胞(CD4^(+)T),购买正常人FLS,应用单钠尿酸盐结晶液刺激正常人FLS构建GA-FLS模型,细胞迁移(transwell)进行CD4^(+)T细胞与GA-FLS共培养,构建miR-23a-3p模拟物(miR-23a-3p mimics)转染至GA-FLS中;黄芩苷作用24 h、48 h和72 h后,细胞计数8(CCK8)检测细胞活力并选取最佳作用浓度和时间;实验分为正常组(GA-FLS)、对照组(CD4^(+)T+GA-FLS)、模型组(GA-CD4^(+)T+GA-FLS)、黄芩苷组(GA-CD4^(+)T+GA-FLS+100μg/ml Baicalin)、miR-23a-3p-NC组(GA-CD4^(+)T+GA-FLS+miR-23a-3p-NC)、miR-23a-3p mimics组(GA-CD4^(+)T+GA-FLS+miR-23a-3p mimics)、黄芩苷miR-23a-3p mimics组(GA-CD4^(+)T+GAFLS+miR-23a-3p mimics+100μg/ml Baicalin);实时定量聚合酶链式反应(RT-qPCR)和免疫印迹(WB)检测miR-23a3p、PTEN、PI3K、AKT、mTOR的表达,酶联免疫吸附(ELISA)测定检测肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、白细胞介素-10(IL-10)的表达。结果:CCK8检测结果显示黄芩苷最佳作用浓度和时间为100μg/ml、48 h。RT-qPCR和WB检测结果显示:模型组miR-23a-3p mRNA、PI3K mRNA、AKT mRNA、mTOR mRNA的表达较正常组、对照组明显升高,差异有统计学意义(P<0.01);而PTEN mRNA组表达明显下降,差异有统计学意义(P<0.01);与miRNA-23a-3p-NC组相比,miR-23a-3p mimics组miRNA-23a-3p mRNA、PI3K mRNA、AKT mRNA、mTOR mRNA的表达明显上升,PTEN mRNA的表达明显下降,差异有统计学意义(P<0.01);与miR-23a3p mimics组相比,黄芩苷miR-23a-3p mimics组miRNA-23a-3p mRNA、PI3K mRNA、AKT mRNA、mTOR mRNA的表达明显下调,PTEN mRNA的表达明显上调,差异有统计学意义(P<0.01)。ELISA检测结果显示:模型组TNF-α、IL1β、IL-6的表达较正常组、对照组明显升高,而IL-10表达明显降低,差异有统计学意义(P<0.01);与miRNA-23a3p-NC组相比,miRNA-23a-3p mimics组TNF-α、IL-1β、IL-6的表达明显上升,IL-10表达明显下降,差异有统计学意义(P<0.01);与miR-23a-3p mimics组相比,黄芩苷miR-23a-3p mimics组TNF-α、IL-1β、IL-6的表达明显下调,IL-10表达明显上调,差异有统计学意义(P<0.01)。结论:黄芩苷可通过下调miR-23a-3p,抑制PTEN/PI3K/AKT/mTOR信号通路的激活,降低痛风性关节炎成纤维样滑膜细胞炎症反应。 展开更多
关键词 痛风性关节炎 成纤维样滑膜细胞 炎症 黄芩苷 miR-23a-3p pten/PI3K/AKT/mtor
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CircRNA ATF6 promotes ovarian cancer cell progression by activating PTEN/mTOR signaling pathway 被引量:1
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作者 LIETING MA MIAOLING LI XINGLONG ZHENG 《BIOCELL》 SCIE 2021年第2期317-321,共5页
Ovarian cancer is a malignant cancer type and affects women’s lives in the world.Circular RNAs(circRNAs)have been involved with the progression of cancers.In our study,we are going to explore the functions of circATF... Ovarian cancer is a malignant cancer type and affects women’s lives in the world.Circular RNAs(circRNAs)have been involved with the progression of cancers.In our study,we are going to explore the functions of circATF6 in ovarian cancer.The qRT-PCR assay was used to detect expressions of genes.Actinomycin D and RNase R treatment were implemented to verify the circular RNA character of circATF6.Besides,Cell proliferation was assessed by colony formation assay and EdU assay.Silenced circATF6 could reduce the proliferation of ovarian cancer cells.In addition,inhibited circATF6 could promote the cell apoptosis and inhibit related proteins in PTEN/mTOR signaling pathway in ovarian cancer.In conclusion,CircRNA ATF6 promotes ovarian cancer cell progression by activating PTEN/mTOR signaling pathway. 展开更多
关键词 CircRNA ATF6 pten/mtor signaling pathway Ovarian cancer
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Echinoside A from Pearsonothuria graeffei Exert the Cytotoxicity to MDA-MB-231 Cells via Mitochondrial Membrane and Modulation of PI3K/Akt/mTOR Pathway
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作者 LI Hongyan CUI Huanhuan +4 位作者 CONG Peixu XU Jie XIE Wancui WANG Yuming XUE Changhu 《Journal of Ocean University of China》 SCIE CAS CSCD 2023年第1期205-212,共8页
A kind of triterpene glycosides echinoside A(EA)was extracted from sea cucumber Pearsonothuria graeffei,and its yield was about 0.78%.The purity of EA was 99.0%,and its molecular weight was 1206 Da.EA was a linear tet... A kind of triterpene glycosides echinoside A(EA)was extracted from sea cucumber Pearsonothuria graeffei,and its yield was about 0.78%.The purity of EA was 99.0%,and its molecular weight was 1206 Da.EA was a linear tetrasaccharide attached to a pentacyclic triterpene aglycon.It inhibited the growth of MDA-MB-231 cells in vitro.The antitumor effect was related to elevate ROS level,decrease mitochondrial membrane potential,enhance caspase-3 expression,induce cells apoptosis and arrest cell cycle at G2/M phase.EA also dose-dependently suppressed the expressions of phophorylation proteins p-PI3K,p-Akt,and p-mTOR as analyzed by western blotting.These results suggested that EA caused MDA-MB-231 cells apoptosis via intrinsic mitochondrial and PI3K/Akt/mTOR pathway.EA can be a potential anti-breast cancer agent to enhance the clinical efficacy. 展开更多
关键词 Pearsonothuria graeffei echinoside A CYTOTOXICITY PI3K/Akt/mtor pathway
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Research progress of TCM regulating mTOR signaling pathway in the treatment of Alzheimer's disease
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作者 LIU Chang‑ning ZHANG Li‑juan +3 位作者 HOU Han‑ru GUAN Xiu‑ju ZHU Ling‑hui WANG Kang‑feng 《Journal of Hainan Medical University》 CAS 2023年第8期65-70,共6页
Alzheimer's disease(AD)is a degenerative disease of the central nervous system.The pathogenesis of AD is complex and diverse,and its occurrence and development is the result of the interaction of multiple factors.... Alzheimer's disease(AD)is a degenerative disease of the central nervous system.The pathogenesis of AD is complex and diverse,and its occurrence and development is the result of the interaction of multiple factors.A number of studies have shown that mTOR signaling pathway is closely related to AD.In recent years,people in exploring relevant methods for the treatment of AD and the process of drugs,more and more studies have found that traditional Chinese medicine compound traditional Chinese medicine monomer,and can be applied to mTOR signaling pathway to improve symptoms in patients with AD.This paper will review the mechanism of action and treatment of TCM in Alzheimer's disease based on mTOR signaling pathway in recent years,so as to provide reference and expand thinking for the prevention and treatment of AD. 展开更多
关键词 Alzheimer's Disease mtor Signaling pathway Traditional Chinese medicine Research progress
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Novel insights into mTOR signalling pathways: A paradigm for targeted tumor therapy
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作者 Oivind Riis Andreas Stensvold +2 位作者 Helge Stene-Johansen Frank Westad Rabia Mehmod 《Cancer Advances》 2023年第17期1-10,共10页
As a crucial protein kinase,the mammalian target of rapamycin(mTOR)intimately controls essential cellular processes like cell development,proliferation,metabolism,and other crucial activities.Different cancers and dis... As a crucial protein kinase,the mammalian target of rapamycin(mTOR)intimately controls essential cellular processes like cell development,proliferation,metabolism,and other crucial activities.Different cancers and disorders have been linked to imbalances in mTOR's regulatory systems.Multiple mTOR inhibitor therapy has recently acquired popularity as a method of treating cancers brought on by abnormal signal transduction pathways.We also explore potential processes behind tumor cell resistance to mTOR inhibitors and suggest workarounds to overcome this challenge.We hold the potential to pioneer cutting-edge methods for tumor therapy by methodically examining the complex mTOR signaling system and its regulatory complexity.Increasing our knowledge of mTOR-related mechanisms not only creates opportunities for cutting-edge methods to target and treat cancers but also has the potential to improve patient outcomes and general quality of life significantly.This review paper explores the most recent developments in understanding mTOR signaling pathways and the use of mTOR inhibitors in treating tumors. 展开更多
关键词 mtor signal transduction pathway TUMOR drug resistance targeted therapy Submit a
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miR-181-5p靶向PTEN/AKT/mTOR通路对氧化应激诱导下人皮肤成纤维细胞自噬及老化的影响
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作者 黄燕 杨艳清 +2 位作者 万睿 周进飞 胡梦 《中国老年学杂志》 CAS 北大核心 2023年第18期4538-4542,共5页
目的探讨miR-181-5p靶向10号染色体上缺失的磷酸酶及张力蛋白同源基因(PTEN)/蛋白激酶B(AKT)/哺乳动物雷帕霉素靶蛋白(mTOR)通路对氧化应激诱导下人皮肤成纤维(HDF)细胞自噬及老化的影响。方法以HDF细胞为研究对象,利用不同浓度H_(2)O_(... 目的探讨miR-181-5p靶向10号染色体上缺失的磷酸酶及张力蛋白同源基因(PTEN)/蛋白激酶B(AKT)/哺乳动物雷帕霉素靶蛋白(mTOR)通路对氧化应激诱导下人皮肤成纤维(HDF)细胞自噬及老化的影响。方法以HDF细胞为研究对象,利用不同浓度H_(2)O_(2)(0、100、200、500μmol/L)处理细胞,通过CCK-8法检测细胞存活率,确定构建细胞老化模型的适宜H_(2)O_(2)浓度,并将该浓度H_(2)O_(2)诱导的HDF细胞命名为H_(2)O_(2)模型细胞;双荧光素酶报告基因实验验证miR-181-5p与PTEN的靶向关系;利用Lipofectamine2000试剂盒对H_(2)O_(2)模型细胞进行转染,细胞分组为:空白组(细胞未转染)、miR-181-5p mimics组、miR-NC组、anti-miR-181-5p组、anti-miR-NC组;荧光定量聚合酶链反应(qRT-PCR)检测细胞中miR-181-5p表达水平;Western印迹检测细胞中PTEN/AKT/mTOR通路相关蛋白、自噬相关蛋白(Beclin)-1、微管相关蛋白轻链(LC)3Ⅱ/Ⅰ表达水平;β-半乳糖苷酶(SA-β-gal)试剂盒观察各组细胞形态及SA-β-gal染色阳性比例。结果随着H_(2)O_(2)浓度的升高,HDF细胞存活率逐渐降低,有统计学差异(P<0.05),H_(2)O_(2)浓度为200μmol/L时,细胞存活率为51.64%,所以选择200μmol/L H_(2)O_(2)作为适宜诱导浓度;与HDF细胞相比,H_(2)O_(2)模型细胞中miR-181-5p、磷酸化(p)-AKT、p-mTOR蛋白表达明显上调,PTEN蛋白表达明显下调(P<0.05);双荧光素酶报告基因实验证实PTEN和miR-181-5p存在靶向关系;与空白组和miR-NC组比较,miR-181-5p mimics组中miR-181-5p、p-AKT、p-mTOR蛋白表达明显上调,PTEN、Beclin-1、LC3Ⅱ/Ⅰ蛋白表达明显下调(P<0.05),细胞排列不规则、变大,轮廓不清楚,折光性差等老化状态更加明显,SA-β-gal染色阳性率显著升高(P<0.05);与空白组和anti-miR-NC组比较,anti-miR-181-5p组中miR-181-5p、p-AKT、p-mTOR蛋白表达明显下调,PTEN、Beclin-1、LC3Ⅱ/Ⅰ蛋白表达明显上调(P<0.05),大多数细胞呈长梭形,轮廓清晰,折光性好,且SA-β-gal染色阳性率显著降低(P<0.05)。结论抑制miR-181-5p可能通过靶向上调PTEN蛋白表达,抑制AKT/mTOR通路,促进细胞自噬,进而延缓氧化应激诱导下HDF细胞老化。 展开更多
关键词 氧化应激 miR-181-5p 10号染色体上缺失的磷酸酶及张力蛋白同源基因(pten)/蛋白激酶B(AKT)/哺乳动物雷帕霉素靶蛋白(mtor)通路 自噬
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PTEN和mTOR信号转导通路在胆管癌发展中作用的研究 被引量:13
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作者 刘民锋 罗剑 +3 位作者 余险峰 唐启彬 陈勇军 邹声泉 《中国普通外科杂志》 CAS CSCD 2006年第4期274-276,共3页
目的研究PI3K/PTEN/AKT/mTOR信号转导通路中mTOR和PTEN蛋白在胆管癌中的表达及其在胆管癌发生、发展中的作用。方法用免疫组织化学方法和RT-PCR法,检测胆管癌中mTOR和PTEN的表达。结果与正常组织相比,免疫组化法和RT-PCR两种方法结果均... 目的研究PI3K/PTEN/AKT/mTOR信号转导通路中mTOR和PTEN蛋白在胆管癌中的表达及其在胆管癌发生、发展中的作用。方法用免疫组织化学方法和RT-PCR法,检测胆管癌中mTOR和PTEN的表达。结果与正常组织相比,免疫组化法和RT-PCR两种方法结果均显示,胆管癌中的mTOR表达明显增加,而PTEN的表达明显下降;两者呈负相关(r=-0.8 6 2,P<0.0 1)。结论PI3K/PTEN/AKT/mTOR信号转导通路中重要的调节位点和节点PTEN在胆管癌中的表达明显降低,而mTOR的表达明显增高。提示该信号转导通路在介导胆管癌的发生、发展的过程中起重要作用。 展开更多
关键词 胆管肿瘤 信号传导 mtor pten
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mTOR和PTEN在非小细胞肺癌组织中的表达及临床意义 被引量:9
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作者 王亮 许绍发 +3 位作者 岳文涛 赵晓婷 张丽娜 王玥 《中国肺癌杂志》 CAS 2010年第7期717-721,共5页
背景与目的mTOR是调节细胞生长和增殖的重要信号转导分子,也是一种蛋白激酶。它通过活化下游的相关的效应蛋白发挥作用。在信号转导通路中PTEN基因可通过对该信号途径的负调控而抑制mTOR的活化。本研究通过分析mTOR信号转导途径中mTOR和... 背景与目的mTOR是调节细胞生长和增殖的重要信号转导分子,也是一种蛋白激酶。它通过活化下游的相关的效应蛋白发挥作用。在信号转导通路中PTEN基因可通过对该信号途径的负调控而抑制mTOR的活化。本研究通过分析mTOR信号转导途径中mTOR和PTEN基因在非小细胞肺癌(non-small cell lung cancer,NSCLC)组织中的表达和临床意义。方法外科手术中获取65例NSCLC组织及30例癌旁组织,RT-PCR技术检测NSCLC组织及癌旁组织中mTOR和PTEN基因的表达水平。结果mTOR在NSCLC组织中表达量(0.23±0.16)显著高于癌旁组(0.12±0.09)(P<0.01),PTEN在NSCLC组织中表达量(0.19±0.28)显著低于癌旁组(0.53±0.28)(P<0.01)。mTOR和PTEN与病人的性别、年龄、病理类型、淋巴结转移情况无关,与病人的肿瘤大小有关。结论mTOR在NSCLC中被激活,PTEN在NSCLC组织表达缺失或减少,mTOR通路的激活和PTEN表达缺失在NSCLC发生发展中起到一定的作用。 展开更多
关键词 mtor pten 逆转录聚合酶链反应 肺肿瘤
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PTEN对K562细胞mTOR调控的研究 被引量:6
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作者 成志勇 杨晓阳 +4 位作者 薛芳 李世辉 姚丽 杜行严 潘崚 《肿瘤》 CAS CSCD 北大核心 2009年第2期139-144,共6页
目的:探讨肿瘤抑制基因PTEN在人慢性粒细胞白血病细胞株K562中对哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)的调控作用,以及雷帕霉素(rapamycin,RAPA)对K562细胞增殖抑制的影响。方法:通过实时荧光定量PCR(real-time ... 目的:探讨肿瘤抑制基因PTEN在人慢性粒细胞白血病细胞株K562中对哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)的调控作用,以及雷帕霉素(rapamycin,RAPA)对K562细胞增殖抑制的影响。方法:通过实时荧光定量PCR(real-time fluorescent quantification PCR,RFQ-PCR)法检测甲磺酸伊马替尼(imatinib mexylate)干预K562细胞后BCR/ABL、PTEN、mTOR mRNA的表达水平及相互关系;Western印迹法检测甲磺酸伊马替尼干预和以腺病毒为载体感染野生型PTEN(Ad-PTEN-GFP)后K562细胞PTEN、Akt和p-Akt的蛋白表达水平;用MTT和FCM方法检测RAPA对不同腺病毒感染组K562细胞增殖及凋亡的影响。结果:格列卫干预K562细胞后,BCR/ABL和mTOR mRNA表达下调,PTEN mRNA表达上调;与感染Ad-GFP组相比,感染Ad-PTEN-GFP组的mTOR mRNA表达下调;Ad-PTEN-GFP感染与10nmol/L RAPA联合作用于K562细胞能够发挥协同作用,对K562细胞的增殖抑制率明显高于单独作用组。结论:PTEN是mTOR的上游调控基因,能够抑制mTOR的表达。RAPA与野生型PTEN一起可以协同抑制K562细胞的增殖。 展开更多
关键词 白血病 实验性 基因表达调控 基因 pten mtor 细胞 K562
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糖尿病大鼠肾组织中PTEN/AKT/mTOR通路对自噬的调控作用 被引量:15
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作者 吴德佩 肖瑛 +4 位作者 张莹莹 曾令萍 石明隽 王圆圆 郭兵 《中国病理生理杂志》 CAS CSCD 北大核心 2016年第11期2015-2019,共5页
目的:观察糖尿病大鼠肾组织中PTEN和自噬水平的变化,探讨糖尿病肾病中PTEN/AKT/m TOR通路对自噬的调控机制。方法:将SD大鼠随机分为正常对照组(NC组)和糖尿病组(DM组),每组各8只。用链脲佐菌素复制DM大鼠模型。于成模后10周处死大鼠后... 目的:观察糖尿病大鼠肾组织中PTEN和自噬水平的变化,探讨糖尿病肾病中PTEN/AKT/m TOR通路对自噬的调控机制。方法:将SD大鼠随机分为正常对照组(NC组)和糖尿病组(DM组),每组各8只。用链脲佐菌素复制DM大鼠模型。于成模后10周处死大鼠后测定相应生化指标和肾脏指数,免疫组化观察肾小管上皮细胞PTEN蛋白的表达部位;Western blotting法检测肾组织LC3、PTEN及PTEN/AKT/m TOR通路的变化;realtime PCR检测肾组织PTEN的mRNA表达水平。结果:DM组的血糖、24 h尿蛋白量和肾脏指数均显著高于NC组(P<0.05)。与NC组相比,DM组大鼠肾组织的LC3I和LC3II水平明显降低(P<0.05)。PTEN主要分布于肾小管上皮细胞中,DM组PTEN蛋白的表达水平明显低于NC组(P<0.05)。DM大鼠肾组织中,PTEN/AKT/m TOR通路的活性增高。结论:糖尿病大鼠肾脏组织中细胞自噬水平下降,而参与自噬调控的PTEN/AKT/m TOR通路活性升高,提示其自噬水平的变化可能受到PTEN/AKT/m TOR通路的调节。 展开更多
关键词 自噬 糖尿病肾病 pten/AKT/mtor信号通路
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细胞角蛋白13通过PTEN抑制PI3K/AKT/mTOR通路增强鼻咽癌HNE1细胞放疗敏感性 被引量:5
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作者 王欢 万佳 +2 位作者 施明 王锦 余宏 《中国肿瘤生物治疗杂志》 CAS CSCD 北大核心 2021年第1期31-36,共6页
目的:探讨细胞角蛋白13(cytokeratin 13,CK13)对鼻咽癌HNE1细胞放疗敏感性的影响及其作用机制。方法:将HNE1细胞分为对照组、anti-CK13#a组及anti-CK13#b组(敲减CK13)、对照组+西罗莫司处理组(100 nmol/L的西罗莫司处理1 h)、anti-CK13... 目的:探讨细胞角蛋白13(cytokeratin 13,CK13)对鼻咽癌HNE1细胞放疗敏感性的影响及其作用机制。方法:将HNE1细胞分为对照组、anti-CK13#a组及anti-CK13#b组(敲减CK13)、对照组+西罗莫司处理组(100 nmol/L的西罗莫司处理1 h)、anti-CK13#a+西罗莫司处理组(100 nmol/L的西罗莫司处理1 h),经放疗处理(200 c Gy/min剂量照射5 min)后,用CCK-8法检测各组细胞的增殖能力,用流式细胞术检测各组细胞的凋亡率,q PCR法检测PI3K/AKT/mTOR信号通路相关基因PTEN的表达,WB法检测PI3K/AKT/mTOR信号通路相关蛋白的表达。结果:经放疗处理后,与对照组相比,敲减CK13后HNE1细胞增殖能力明显增强(P<0.01),细胞凋亡率明显降低(P<0.01);细胞中c-caspase-3和γH2AX的表达明显降低(均P<0.01)、p-AKT和p-S6K表达明显升高(P<0.01)、PTEN蛋白表达明显降低(P<0.01)。敲减CK13+西罗莫司(PI3K/AKT/mTOR信号通路抑制剂)处理可以回复敲减CK13导致的细胞增殖能力增强(P<0.05)和细胞凋亡率降低(P<0.01)。结论:敲减CK13通过下调PTEN蛋白水平进而增强PI3K/AKT/mTOR信号通路活性,最终降低HNE1细胞的放疗敏感性。 展开更多
关键词 鼻咽癌 HNE1细胞 放疗 细胞角蛋白13 pten PI3K/AKT/mtor信号通路
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PTEN/Akt/mTOR通路增加K562/ADM细胞化疗敏感性 被引量:3
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作者 成志勇 王素云 +5 位作者 卞永生 温省初 杨宁 高晓丽 韩英 潘崚 《基础医学与临床》 CSCD 北大核心 2012年第1期49-55,共7页
目的探讨K562/ADM细胞系中PTEN/Akt/mTOR信号通路对不同化疗药物敏感性的影响。方法 K562/ADM细胞分为未转染组、转染野生型PTEN组(Ad-PTEN-GFP)、转染空载体组(Ad-GFP),并与不同浓度雷帕霉素或三氧化二砷(As2O3)联合作用。通过MTT法检... 目的探讨K562/ADM细胞系中PTEN/Akt/mTOR信号通路对不同化疗药物敏感性的影响。方法 K562/ADM细胞分为未转染组、转染野生型PTEN组(Ad-PTEN-GFP)、转染空载体组(Ad-GFP),并与不同浓度雷帕霉素或三氧化二砷(As2O3)联合作用。通过MTT法检测细胞增殖,流式细胞术检测细胞凋亡率,荧光定量PCR检测PTEN、mTOR、BCL-2及BAX mRNA水平,Western blot检测PTEN及Akt、p-Akt蛋白水平。结果野生型PTEN对K562/ADM细胞最大增殖抑制率为32.3%,与未转染组及Ad-GFP组相比,Ad-PTEN-GFP组mTOR mRNA和p-Akt蛋白明显减低;雷帕霉素与As2O3联合应用后细胞增殖明显受抑,凋亡率(28.61%±1.46%)明显高于单药作用组(P<0.05),BCL-2 mRNA表达降低,BAX mRNA表达增加,以联合干预组最为明显。结论 PTEN/Akt/mTOR信号传导通路能够增加K562/ADM细胞对雷帕霉素及As2O3的敏感性。 展开更多
关键词 AKT pten mtor 雷帕霉素 三氧化二砷
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