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The Antidepressant Mechanism of JiaWeiWenDan Decoction Regulating p38MAPK-ERK5 Signal Transduction Pathway
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作者 Yue Gao Qi Zhang +1 位作者 Li Wu Jianye Dai 《Journal of Biosciences and Medicines》 2023年第4期199-207,共9页
Objective: To investigate the anti-depression mechanism of JiaWeiWenDan Decoction in regulating p38MAPK-ERK5 signal transduction pathway. Methods: Depression model rats were randomly divided into Blank Control Group, ... Objective: To investigate the anti-depression mechanism of JiaWeiWenDan Decoction in regulating p38MAPK-ERK5 signal transduction pathway. Methods: Depression model rats were randomly divided into Blank Control Group, Model Control Group, Chinese Medicine Treatment Group, and Western Medicine Treatment Group (hereinafter referred to as Blank Group, Model Group, Chinese Medicine Group, and Western Medicine Group), with 48 rats in each group. The mice were treated with p38MAPK-ERK5 on the 7th day, 14th day and 21st day, respectively, and the mice were treated for 28 days. The key targets and cytokines in p38MAPK-ERK5 signal transduction pathway were detected. Results: Compared with the Blank Group, the expression of p38MAPKmRNA in the hippocampus of the Model Group was increased. The Chinese Medicine Group and Western Medicine Group could reduce the expression of p38MAPK mRNA (P P P P Conclusion: The anti-inflammatory effect of JiaWeiWenDan Decoction may be related to the regulation of p38MAPK-ERK5 signaling pathway. With the advance of the treatment week, the best effect was obtained when the treatment was started on the 7th day of modeling. 展开更多
关键词 JiaWeiWenDan Decoction DEPRESSION p38MAPK-ERK5 Signal transduction pathway
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Interaction of major genes predisposing to hepatocellular carcinoma with genes encoding signal transduction pathways influences tumor phenotype and prognosis 被引量:5
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作者 Francesco Feo Maddalena Frau Rosa Maria Pascale 《World Journal of Gastroenterology》 SCIE CAS CSCD 2008年第43期6601-6615,共15页
Studies on rodents and humans demonstrate an inherited predisposition to hepatocellular carcinoma (HCC). Analysis of the molecular alterations involved in the acquisition of a phenotype resistant or susceptible to h... Studies on rodents and humans demonstrate an inherited predisposition to hepatocellular carcinoma (HCC). Analysis of the molecular alterations involved in the acquisition of a phenotype resistant or susceptible to hepatocarcinogenesis showed a deregulation of G1 and S phases in HCC of genetically susceptible F344 rats and a G1-S block in lesions of resistant Brown norway (BN) rats. Unrestrained extracellular signal-regulated kinase (ERK) activity linked to proteasomal degradation of dual-specificity phosphatase 1 (DUSP1), a specific ERK inhibitor, by the CKS1-SKP2 ubiquitin ligase complex occurs in more aggressive HCC of F344 rats and humans. This mechanism is less active in HCC of BN rats and human HCC with better prognosis. Upregulation of iNos cross-talk with IKK/NF-KB and RAS/ERK pathways occurs in rodent liver lesions at higher levels in the most aggressive models represented by HCC of F344 rats and c-Myc-TGF-α transgenic mice. iNOS, IKK/NF-κB, and RAS/ERK upregulation is highest in human HCC with a poorer prognosis and positively correlates with tumor proliferation, genomic instability and microvascularization, and negatively with apoptosis. Thus, cell cycle regulation and the activity of signal transduction pathways seem to be modulated by HCC modifier genes, and differences in their efficiency influence the susceptibility to hepatocarcinogenesis and probably the prognosis of human HCC. 展开更多
关键词 HEPATOCARCINOGENESIS Genetic predisposition Polygenic disease Redifferentiation Signal transduction pathways Cell cycle Cell proliferation Apoptosis Proteasomal degradation
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Differential Signal Transduction Pathways Mediating the Actions of Two Native GnRH Peptides on Pituitary GTH and GH Secretion in Goldfish
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作者 JongP.Chang RichardM.Jobin +3 位作者 FredrickVanGoor AndersonO.L.Wong RafeGarofalo CatherineM.Neumann 《中山大学学报论丛》 1995年第3期190-191,共2页
关键词 GTH GNRH Differential Signal transduction pathways Mediating the Actions of Two Native GnRH Peptides on Pituitary GTH and GH Secretion in Goldfish GH
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Sericin can reduce hippocampal neuronal apoptosis by activating the Akt signal transduction pathway in a rat model of diabetes mellitus 被引量:4
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作者 Zhihong Chen Yaqiang He +3 位作者 Chengjun Song Zhijun Dong Zhejun Su Jingfeng Xue 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第3期197-201,共5页
In the present study, a rat model of type 2 diabetes mellitus was established by continuous peritoneal injection of streptozotocin. Following intragastric perfusion of sericin for 35 days, blood glucose levels signifi... In the present study, a rat model of type 2 diabetes mellitus was established by continuous peritoneal injection of streptozotocin. Following intragastric perfusion of sericin for 35 days, blood glucose levels significantly reduced, neuronal apoptosis in the hippocampal CA1 region decreased, hippocampal phosphorylated Akt and nuclear factor kappa B expression were enhanced, but Bcl-xL/Bcl-2 associated death promoter expression decreased. Results demonstrated that sericin can reduce hippocampal neuronal apoptosis in a rat model of diabetes mellitus by regulating abnormal changes in the Akt signal transduction pathway. 展开更多
关键词 SERICIN type 2 diabetes mellitus HIPPOCAMPUS apoptosis Akt signal transduction pathway neural regeneration
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Rho/Rock signal transduction pathway is required for MSC tenogenic differentiation 被引量:6
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作者 Edward Maharam Miguel Yaport +5 位作者 Nathaniel L Villanueva Takintope Akinyibi Damien Laudier Zhiyong He Daniel J Leong Hui B Sun 《Bone Research》 SCIE CAS CSCD 2015年第3期173-181,共9页
Mesenchymal stem cell (MSC)-based treatments have shown promise for improving tendon healing and repair. MSCs have the potential to differentiate into multiple lineages in response to select chemical and physical st... Mesenchymal stem cell (MSC)-based treatments have shown promise for improving tendon healing and repair. MSCs have the potential to differentiate into multiple lineages in response to select chemical and physical stimuli, including into tenocytes. Cell elongation and cytoskeletal tension have been shown to be instrumental to the process of MSC differentiation. Previous studies have shown that inhibition of stress fiber formation leads MSCs to default toward an adipogenic lineage, which suggests that stress fibers are required for MSCs to sense the environmental factors that can induce differentiation into tenocytes. As the Rho/ROCK signal transduction pathway plays a critical role in both stress fiber formation and in cell sensation, we examined whether the activation of this pathway was required when inducing MSC tendon differentiation using rope-like silk scaffolds. To accomplish this, we employed a loss-of-function approach by knocking out ROCK, actin and myosin (two other components of the pathway) using the specific inhibitors Y-27632, Latrunculin A and blebbistatin, respectively. We demonstrated that independently disrupting the cytoskeleton and the Rho/ ROCK pathway abolished the expression of tendon differentiation markers and led to a loss of spindle morphology. Together, these studies suggest that the tension that is generated by MSC elongation is essential for MSC teno-differentiation and that the Rho/ROCK pathway is a critical mediator of tendon differentiation on rope-like silk scaffolds. 展开更多
关键词 MSCS FIGURE Rho/Rock signal transduction pathway is required for MSC tenogenic differentiation
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Role of Toll-like receptor 4 and Janus kinase and signal transducer and activator of transcription signal transduction pathway in sepsis-induced brain damage 被引量:1
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作者 Haiyan Yin Jianrui Wei +2 位作者 Rui Zhang Xiaoling Ye Youfeng Zhu 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第32期2511-2515,共5页
The Janus kinase and signal transducer and activator of transcription (JAK/STAT) signal transduction pathway is involved in sepsis-induced functional damage to the heart, liver, kidney, and other organs. However, th... The Janus kinase and signal transducer and activator of transcription (JAK/STAT) signal transduction pathway is involved in sepsis-induced functional damage to the heart, liver, kidney, and other organs. However, the cellular and molecular mechanisms underlying sepsis-induced brain damage remain elusive. In the present study, we found severe loss of neurons in the hippocampal CA1 region in rats with sepsis-induced brain damage following intraperitoneal injection of endotoxin, The expression of toll-like receptor 4, tumor necrosis factor a, and interleukin-6 was significantly increased in brain tissues following lipopolysaccharide exposure. AG490 (JAK2 antagonist) and rapamycin (STAT3 antagonist) significantly reduced neuronal loss and suppressed the increased expression of toll-like receptor 4, tumor necrosis factor a, and interleukin-6 in the hippocampal CA1 region in sepsis-induced brain damaged rats. Overall, these data suggest that blockade of the JAK/STAT signal transduction pathway is neuroprotective in sepsis-induced brain damage via the inhibition of toll-like receptor 4, tumor necrosis factor a, and interleukin-6 exoression. 展开更多
关键词 brain damage Janus kinase and signal transducer and activator of transcription SEPSIS signal transduction pathway Toll-like receptor 4
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Involvement of M3 Cholinergic Receptor Signal Transduction Pathway in Regulation of the Expression of Chemokine MOB-1, MCP-1 Genes in Pancreatic Acinar Cells 被引量:1
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作者 郑海 陈道达 +1 位作者 张景輝 田原 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2004年第2期140-143,157,共5页
Whether M3 cholinergic receptor signal transduction pathway is involved in regulation of the activation of NF-κB and the expression of chemokine MOB-1, MCP-1genes in pancreatic acinar cells was investigated. Rat panc... Whether M3 cholinergic receptor signal transduction pathway is involved in regulation of the activation of NF-κB and the expression of chemokine MOB-1, MCP-1genes in pancreatic acinar cells was investigated. Rat pancreatic acinar cells were isolated, cultured and treated with carbachol, atropine and PDTC in vitro. The MOB-1 and MCP-1 mRNA expression was detected by using RT-PCR. The activation of NF-κB was monitored by using electrophoretic mobility shift assay. The results showed that as compared with control group, M3 cholinergic receptor agonist (10 -3 mol/L, 10 -4 mol/L carbachol) could induce a concentration-dependent and time-dependent increase in the expression of MOB-1, MCP-1 mRNA in pancreatic acinar cells. After treatment with 10 -3 mol/L carbachol for 2 h, the expression of MOB-1, MCP-1 mRNA was strongest. The activity of NF-κB in pancreatic acinar cells was significantly increased (P<0.01) after treated with M3 cholinergic receptor agonist (10 -3 mol/L carbachol) in vitro for 30 min. Either M3 cholinergic receptor antagonist (10 -5 mol/L atropine) or NF-κB inhibitor (10 -2 mol/L PDTC) could obviously inhibit the activation of NF-κB and the chemokine MOB-1, MCP-1 mRNA expression induced by carbachol (P<0.05). This inhibitory effect was significantly increased by atropine plus PDTC (P<0.01). The results of these studies indicated that M3 cholinergic receptor signal transduction pathway was likely involved in regulation of the expression of chemokine MOB-1 and MCP-1genes in pancreatic acinar cells in vitro through the activation of NF-κB. 展开更多
关键词 pancreatic acinar cell M3 cholinergic receptor signal transduction pathway CHEMOKINE NF-κB
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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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Mitogen activated protein kinase signaling pathways participate in the active principle region of Buyang Huanwu decoction-induced differentiation of bone marrow mesenchymal stem cells 被引量:2
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作者 Jinghui Zheng Jian Liang +6 位作者 Xin Deng Xiaofeng Chen Fasheng Wu Xiaofang Zhao Yuan Luo Lei Fu Zuling Jiang 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第18期1370-1377,共8页
Our preliminary studies confirmed that an active principle region of Buyang Huanwu decoction, comprising alkaloid, polysaccharide, aglycon, glucoside and volatile oil, can induce bone marrow mesenchymal stem cell diff... Our preliminary studies confirmed that an active principle region of Buyang Huanwu decoction, comprising alkaloid, polysaccharide, aglycon, glucoside and volatile oil, can induce bone marrow mesenchymal stem cell differentiation into neurons. Mitogen-activated protein kinase signaling was identified as one of the key pathways underlying this differentiation process. The present study shows phosphorylated extracellular signal-regulated protein kinase and phosphorylated p38 protein expression was increased after differentiation. Cellular signaling pathway blocking agents, PD98059 and SB203580, inhibited extracellular signal-regulated protein kinase and p38 in mitogen-activated protein kinase signaling pathways respectively, mRNA and protein expression of the neuronal marker, neuron specific enolase, and neural stem cell marker, nestin, were decreased in bone marrow mesenchymal stem cells after treatment with the active principle region of Buyang Huanwu decoction. Experimental findings indicate that, extracellular signal-regulated protein kinase and p38 in mitogen-activated protein kinase signaling pathways participate in bone marrow mesenchymal stem cell differentiation into neuron-like cells, induced by the active principle region of Buyang Huanwu decoction. 展开更多
关键词 Buyang Huanwu decoction bone marrow mesenchymal stem ceils extracellular signal-regulatedprotein kinase mitogen-activated protein kinase signaling pathway neuron specific enolase NESTIN cell signal transduction pathway neural regeneration
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Influence of electroacupuncture on mitogen-activated protein kinase signal transduction in a rat model of cerebral ischemia/reperfusion 被引量:1
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作者 Zhongren Li Meihong Shen +1 位作者 Wenmin Niu Xiaoren Xiang 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第30期2362-2366,共5页
Following electroacupuncture at Baihui (DU 20) and Dazhui (DU 14) in a rat model of cerebral ischemia/reperfusion, extracellular-signal-regulated kinase expression in cerebral cortex and corpus striatum, serum glu... Following electroacupuncture at Baihui (DU 20) and Dazhui (DU 14) in a rat model of cerebral ischemia/reperfusion, extracellular-signal-regulated kinase expression in cerebral cortex and corpus striatum, serum glutathione reductase, glutathione peroxidase activity, and serum glutathione content were elevated, and neurobehavioral scores improved. However, these effects were antagonized by mitogen-activated protein kinase inhibitor PD98059. Results indicated that electroacupuncture reversed free radical chain reactions and oxidative stress injury caused by cerebral ischemia/reperfusion, thereby providing neuroprotection. This process could correlate with the mitogen-activated protein kinase signal transduction pathway. 展开更多
关键词 anti-oxidative stress cerebral ischemia/reperfusion ELECTROACUPUNCTURE mitogen-activated protein kinase pathway signal transduction
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Comparative analysis of various modularization algorithms and species specific study of VEGF signaling pathways 被引量:2
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作者 Namrata Tomar Losiana Nayak Rajat K. De 《Journal of Biomedical Science and Engineering》 2010年第10期931-942,共12页
In biology, signal transduction refers to a process by which a cell converts one kind of signal or stimulus into another. It involves ordered sequences of biochemical reactions inside the cell. These cascades of react... In biology, signal transduction refers to a process by which a cell converts one kind of signal or stimulus into another. It involves ordered sequences of biochemical reactions inside the cell. These cascades of reactions are carried out by enzymes and activated by second messengers. Signal transduction pathways are complex in nature. Each pathway is responsible for tuning one or more biological functions in the intracellular environment as well as more than one pathway interact among themselves to carry forward a single biological function. Such kind of behavior of these pathways makes understanding difficult. Hence, for the sake of simplicity, they need to be partitioned into smaller modules and then analyzed. We took VEGF signaling pathway, which is responsible for angiogenesis for this kind of modularized study. Modules were obtained by applying the algorithm of Nayak and De (Nayak and De, 2007) for different complexity values. These sets of modules were compared among themselves to get the best set of modules for an optimal complexity value. The best set of modules compared with four different partitioning algorithms namely, Farhat’s (Farhat, 1998), Greedy (Chartrand and Oellermann, 1993), Kernighan-Lin’s (Kernighan and Lin, 1970) and Newman’s community finding algorithm (Newman, 2006). These comparisons enabled us to decide which of the aforementioned algorithms was the best one to create partitions from human VEGF signaling pathway. The optimal complexity value, on which the best set of modules was obtained, was used to get modules from different species for comparative study. Comparison among these modules would shed light on the trend of development of VEGF signaling pathway over these species. 展开更多
关键词 Signal transduction pathway VEGF pathway Complexity Value KEGG Database MODULARIZATION Newman’s Community Finding ALGORITHM Kernighan-Lin’s ALGORITHM Farhat’s ALGORITHM and GREEDY Algorithm.
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YWHAH activates the HMGA1/PI3K/AKT/mTOR signaling pathway by positively regulating Fra-1 to affect the proliferation of gastric cancer cells
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作者 JUNYU HE FENG ZENG +5 位作者 XI JIN LIN LIANG MENGXIANG GAO WENTAO LI GUIYUAN LI YANHONG ZHOU 《Oncology Research》 SCIE 2023年第4期615-630,共16页
Fos-related antigen 1(Fra-1)is a nuclear transcription factor that regulates cell growth,differentiation,and apoptosis.It is involved in the proliferation,invasion,apoptosis and epithelial mesenchymal transformation o... Fos-related antigen 1(Fra-1)is a nuclear transcription factor that regulates cell growth,differentiation,and apoptosis.It is involved in the proliferation,invasion,apoptosis and epithelial mesenchymal transformation of malignant tumor cells.Fra-1 is highly expressed in gastric cancer(GC),affects the cycle distribution and apoptosis of GC cells,and participates in GC occurrence and development.However,the detailed mechanism of Fra-1 in GC is unclear,such as the identification of Fra-1-interacting proteins and their role in GC pathogenesis.In this study,we identified tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein eta(YWHAH)as a Fra-1-interacting protein in GC cells using co-immunoprecipitation combined with liquid chromatography-tandem mass spectrometry.Experiments showed that YWHAH positively regulated Fra-1 mRNA and protein expression,and affected GC cell proliferation.Whole proteome analysis showed that Fra-1 affected the activity of the high mobility group AT-hook 1(HMGA1)/phosphatidylinositol-4,5-bisphosphate 3-kinase(PI3K)/protein kinase B(AKT)/mechanistic target of rapamycin(mTOR)signaling pathway in GC cells.Western blotting and flow cytometry confirmed that YWHAH activated HMGA1/PI3K/AKT/mTOR signaling pathway by positively regulating Fra-1 to affect GC cell proliferation.These results will help to discover new molecular targets for the early diagnosis,treatment,and prognosis prediction of GC. 展开更多
关键词 Gastric cancer Fra-1 YWHAH Signal transduction pathway Cell proliferation
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Phosphorylated protein chip combined with artificial intelligence tools for precise drug screening
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作者 Katsuhisa Horimoto Yuki Suyama +7 位作者 Tadamasa Sasaki Kazuhiko Fukui Lili Feng Meiling Sun Yamin Tang Yixuan Zhang Dongyin Chen Feng Han 《Journal of Biomedical Research》 CAS CSCD 2024年第3期195-205,共11页
We have developed a protein array system,named"Phospho-Totum",which reproduces the phosphorylation state of a sample on the array.The protein array contains 1471 proteins from 273 known signaling pathways.Ac... We have developed a protein array system,named"Phospho-Totum",which reproduces the phosphorylation state of a sample on the array.The protein array contains 1471 proteins from 273 known signaling pathways.According to the activation degrees of tyrosine kinases in the sample,the corresponding groups of substrate proteins on the array are phosphorylated under the same conditions.In addition to measuring the phosphorylation levels of the 1471 substrates,we have developed and performed the artificial intelligence-assisted tools to further characterize the phosphorylation state and estimate pathway activation,tyrosine kinase activation,and a list of kinase inhibitors that produce phosphorylation states similar to that of the sample.The Phospho-Totum system,which seamlessly links and interrogates the measurements and analyses,has the potential to not only elucidate pathophysiological mechanisms in diseases by reproducing the phosphorylation state of samples,but also be useful for drug discovery,particularly for screening targeted kinases for potential drug kinase inhibitors. 展开更多
关键词 Phospho-Totum protein array signal transduction pathways artificial intelligence tools drug screening
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The JNK Pathway and Neuronal Migration 被引量:1
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作者 孙一明 杨涛 许执恒 《Journal of Genetics and Genomics》 SCIE CAS CSCD 北大核心 2007年第11期957-965,共9页
The c-Jun N-terminal kinases (JNKs) are important regulators of a variety of physiological and pathological processes both in the central and in the peripheral nervous systems. JNKs are considered as crucial mediato... The c-Jun N-terminal kinases (JNKs) are important regulators of a variety of physiological and pathological processes both in the central and in the peripheral nervous systems. JNKs are considered as crucial mediators of neuronal cell death in response to stress and injury. However, recent studies have provided substantial evidence that the JNK pathway plays an important role in neuronal migration. Here, we will give a brief introduction of the JNK signaling pathway and put more emphasis on its role in nettronal migration. 展开更多
关键词 JNK pathway neuronal migration signal transduction
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Functional Insights of Plant GSK3-like Kinases: Multi-Taskers in Diverse Cellular Signal Transduction Pathways 被引量:18
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作者 Ji-Hyun Youn Tae-Wuk Kim 《Molecular Plant》 SCIE CAS CSCD 2015年第4期552-565,共14页
The physiological importance of GSK3-like kinases in plants emerged when the functional role of plant GSK3-like kinases represented by BIN2 was first elucidated in the brassinosteroid (BR)-regulated signal transduct... The physiological importance of GSK3-like kinases in plants emerged when the functional role of plant GSK3-like kinases represented by BIN2 was first elucidated in the brassinosteroid (BR)-regulated signal transduction pathway. While early studies focused more on understanding how GSK3-like kinases regulate BR signaling, recent studies have implicated many novel substrates of GSK3-like kinases that are involved in a variety of cellular processes as well as BR signaling. Plant GSK3-like kinases play diverse roles in physiological and developmental processes such as cell growth, root and stomatal cell development, flower development, xylem differentiation, light response, and stress responses. Here, we review the progress made in recent years in understanding the versatile functions of plant GSK3-like kinases. Based on the relationship between GSK3-like kinases and their newly identified substrates, we discuss the physiological and biochemical relevance of various cellular signaling mediated by GSK3-like kinases in plants. 展开更多
关键词 GSK3-like kinases BRASSINOSTEROIDS signal transduction pathway ARABIDOPSIS rice
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Activation of the PI3K/AKT pathway mediates FSH-stimulated VEGF expression in ovarian serous cystadenocarclnoma 被引量:17
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作者 Yan Huang Keqin Hua +6 位作者 Xianrong Zhou Hongyan Jin Xiaojun Chen Xin Lu Yinhua Yu Xiliang Zha Youji Feng 《Cell Research》 SCIE CAS CSCD 2008年第7期780-791,共12页
There is evidence to suggest that follicle-stimulating hormone (FSH) can facilitate the neovascularization of ovarian cancers by increasing vascular endothelial growth factor (VEGF) expression in cancer cells, alt... There is evidence to suggest that follicle-stimulating hormone (FSH) can facilitate the neovascularization of ovarian cancers by increasing vascular endothelial growth factor (VEGF) expression in cancer cells, although the underlying molecular mechanism of this process is not well known. Therefore, we investigated the effect of FSH on VEGF expression in the ovarian cancer cell lines SKOV-3 and ES-2. Treatment with FSH significantly increased VEGF expression in a dose- and time-dependent manner. In addition, FSH treatment enhanced the expression of survivin and hypoxlainducible factor-1 (HIF-1α). Knockdown of survivin or HIF-1α suppressed VEGF expression, but only knockdown of survivin inhibited FSH-stimulated VEGF expression. Pretreatment with LY294002, a phosphoinositide 3-kinase (PI3K)/AKT inhibitor, neutralized the enhanced expression of survivin induced by FSH, but treatment with U0126, a mitogen-activated protein kinase/extracellular signal-regulated kinase inhibitor, had no such effect. We further showed that ovarian serous cystadenocarcinoma samples had much higher incidence of positive AKT and phosphorylated AKT (pAKT) protein staining than did benign ovarian cystadenoma samples (p 〈 0.01). The 5-year survival rate was only about 15% in patients with ovarian serous cystadenocarcinoma who had AKT and pAKT expression, whereas it was about 80% in those who did not have AKT or pAKT expression. Taken together, these results indicate that FSH increases the expression of VEGF by upregulating the expression of survivin, which is activated by the PI3K/AKT signaling pathway. Understanding the role of the PI3K/AKT pathway in FSH-stimulated expression of survivin and VEGF will be beneficial for evaluating the prognosis for patients with ovarian serous cystadenocarcinoma and for pursulug effective treatment against this disease. 展开更多
关键词 FSH VEGF SURVIVIN PI3K/AKT signal transduction pathway ovarian serous cystadenocarcinoma
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Research progress in the radioprotective effect of the canonical Wnt pathway 被引量:2
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作者 Jin-Feng Wang Chao Liu +1 位作者 Qu Zhang Guan-Hong Huang 《Cancer Biology & Medicine》 SCIE CAS CSCD 2013年第2期61-71,共11页
Irradiation from diverse sources is ubiquitous and closely associated with human activities. Radiation therapy (RT), an important component of multiple radiation origins, is a common therapeutic modality for cancer. M... Irradiation from diverse sources is ubiquitous and closely associated with human activities. Radiation therapy (RT), an important component of multiple radiation origins, is a common therapeutic modality for cancer. More importantly, RT provides significant contribution to oncotherapy by killing tumor cells. However, during the course of therapy, irradiation of normal tissues can result in a wide range of side effects, including self-limited acute toxicities, mild chronic symptoms, or severe organ dysfunction. Although numerous promising radioprotective agents have emerged, only a few have successfully entered the market because of various limitations. At present, the widely accepted hypothesis for protection against radiation-caused injury involves the Wnt canonical pathway. Activating the Wnt/β-catenin signaling pathway may protect the salivary gland, oral mucosa, and gastrointestinal epithelium from radiation damage. The underlying mechanisms include inhibiting apoptosis and preserving normal tissue functions. However, aberrant Wnt signaling underlies a wide range of pathologies in humans, and its various components contribute to cancer. Moreover, studies have suggested that Wnt/ β-catenin signaling may lead to radioresistance of cancer stem cell. These facts markedly complicate any definition of the exact function of the Wnt pathway. 展开更多
关键词 Signaling transduction canonical Wnt pathway ^-catenin RADIOPROTECTION RADIATION
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Adenosine triphosphate promotes locomotor recovery after spinal cord injury by activating mammalian target of rapamycin pathway in rats 被引量:3
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作者 Zhengang Sun Lingyun Hu +4 位作者 Yimin Wen Keming Chen Zhenjuan Sun Haiyuan Yue Chao Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2013年第2期101-110,共10页
The mammalian target of rapamycin (mTOR) pathway plays an important role in neuronal growth, proliferation and differentiation. To better understand the role of mTOR pathway involved in the induction of spinal cord ... The mammalian target of rapamycin (mTOR) pathway plays an important role in neuronal growth, proliferation and differentiation. To better understand the role of mTOR pathway involved in the induction of spinal cord injury, rat models of spinal cord injury were established by modified Allen's stall method and interfered for 7 days by intraperitoneal administration of mTOR activator adenosine triphosphate and mTOR kinase inhibitor rapamycin. At 1-4 weeks after spinal cord injury induction, the Basso, Beattie and Bresnahan locomotor rating scale was used to evaluate rat locomotor function, and immunohistochemical staining and western blot analysis were used to detect the expression of nestin (neural stem cell marker), neuronal nuclei (neuronal marker), neuron specific enolase, neurofilament protein 200 (axonal marker), glial fibrillary acidic protein (astrocyte marker), Akt, mTOR and signal transduction and activator of transcription 3 (STAT3). Results showed that adenosine triphosphate-mediated Akt/mTOR/STAT3 pathway increased endogenous neural stem cells, induced neurogenesis and axonal growth, inhibited excessive astrogliosis and improved the locomotor function of rats with spinal cord injury. 展开更多
关键词 neural regeneration spinal cord injury serine/threonine-specific protein kinase mammalian target ofrapamycin pathway signal transduction and activator of transcription 3 adenosine triphosphate signal pathway rapamycin photographs-containing paper NEUROREGENERATION
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TGF-β1/SMAD SIGNALING PATHWAY MEDIATES p53-DEPENDENT APOPTOSIS IN HEPATOMA CELL LINES 被引量:2
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作者 Chun-lei Wang Yuan-lian Wan +1 位作者 Yu-cun Liu Zhi-qiang Huang 《Chinese Medical Sciences Journal》 CAS CSCD 2006年第1期33-35,共3页
Objective To determine whether transforming growth factor betal (TGF-β1)/Smad signaling pathway mediates p53-dependent apoptosis in hepatoma cell lines.Methods Three human hepatic carcinoma cell lines, HepG2, Huh-7, ... Objective To determine whether transforming growth factor betal (TGF-β1)/Smad signaling pathway mediates p53-dependent apoptosis in hepatoma cell lines.Methods Three human hepatic carcinoma cell lines, HepG2, Huh-7, and Hep3B, were used in this study.TGF-β1-induced apoptosis in hepatic carcinoma cell lines was analyzed using TUNEL assay.For identifying the mechanism of apoptosis induced by TGF-β1, cell lines were transfected with a TGF-β1-inducible luciferase reportor plasmid containing Smad4 binding elements.After transfection, cells were treated with TGF-β1, then assayed for luciferase activity.Results The apoptosis rate of HepG2 cell lines (48.51%± 8.21%) was significantly higher than control ( 12.72%±2.18%, P<0.05).But TGF-β1 was not able to induce apoptosis of Huh-7 and Hep3B cell lines.The relative luciferase activity of TGF-β1-treated HepG2 cell lines (4.38) was significantly higher than control (1.00, P< 0.05).But the relative luciferase activity of TGF-β1-treated Huh-7 and Hep3B cell lines less increased compared with control.Conclusions HepG2 cells seem to be highly susceptible to TGF-β1-induced apoptosis compared with Hep3B and Huh-7 cell lines.Smad4 is a central mediator of TGF-β1 signaling transdution pathway.TGF-β1/Smad signaling pathway might mediate p53-dependent apoptosis in hepatoma cell lines. 展开更多
关键词 transforming growth factor-β1 APOPTOSIS hepatoma cell line signal transduction pathway
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Function of the CaMKII-ryanodine receptor signaling pathway in rabbits with left ventricular hypertrophy and triggered ventricular arrhythmia 被引量:1
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作者 Jun Ke Xing Xiao +6 位作者 Feng Chen Li He Mu-sen Dai Xiao-ping Wang Bing Chen Min Chen Cun-tai Zhang 《World Journal of Emergency Medicine》 CAS 2012年第1期65-70,共6页
BACKGROUND:Calcium calmodulin-dependent kinase II(CaMKII) can be more active in patients with left ventricular hypertrophy(LVH),which in turn causes phosphorylation of ryanodine receptors,resulting in inactivation and... BACKGROUND:Calcium calmodulin-dependent kinase II(CaMKII) can be more active in patients with left ventricular hypertrophy(LVH),which in turn causes phosphorylation of ryanodine receptors,resulting in inactivation and the instability of intracellular calcium homeostasis.The present study aimed to determine the effect of CaMKII-ryanodine receptor pathway signaling in rabbits with left ventricular hypertrophy and triggered ventricular arrhythmia.METHODS:Forty New Zealand rabbits were randomized into four groups(10 per group):sham group,LVH group,KN-93 group(LVH+KN-93),and ryanodine group(LVH+ryanodine).Rabbits in the LVH,KN-93,and ryanodine groups were used to establish a left ventricular hypertrophy model by the coarctation of the abdominal aorta,while those in the sham group did not undergo the coarctation.After eight weeks,action potentials(APs) were recorded simultaneously in the endocardium and epicardium,and a transmural electrocardiogram(ECG) was also recorded in the rabbit left ventricular wedge model.Drugs were administered to the animals in the KN-93 and ryanodine groups,and the frequency of triggered APs and ventricular tachycardia was recorded after the rabbits were given isoprenaline(1 μmol/L) and high-frequency stimulation.RESULTS:The frequency(animals/group) of triggered APs was 0/10 in the sham group,10/10 in the LVH group,4/10 in the KN-93 group,and 1/10 in the ryanodine group.The frequencies of ventricular tachycardia were 0/10,9/10,3/10,and 1/10,respectively.The frequencies of polymorphic ventricular tachycardia or ventricular fibrillation were 0/10,7/10,2/10,and 1/10,respectively.The frequencies of triggered ventricular arrhythmias in the KN-93 and ryanodine groups were much lower than those in the LVH group(P<0.05).CONCLUSIONS:KN-93 and ryanodine can effectively reduce the occurrence of triggered ventricular arrhythmia in rabbits with LVH.The CaMKII-ryanodine signaling pathway can be used as a new means of treating ventricular arrhythmia. 展开更多
关键词 CAMKII Ryanodine receptors Signaling transduction pathway Triggered actionpotential Ventricular arrhythmia Left ventricular hypertrophy
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