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Trans-10,cis-12, not cis-9,trans-11, conjugated linoleic acid decreases ErbB3 expression in HT-29 human colon cancer cells

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World Journal of Gastroenterology 2005年第33期11卷 5142-5150页

作者： Han Jin Cho Woo Kyoung Kim Jae In Jung Eun Ji Kim Soon Sung Lim Dae Young Kwon Jung Han Yoon Park Department of Food Science and Nutrition Hallym University Chuncheon 200-702 Korea Department of Food Science and Nutrition Dankook University Seoul 140-714 Korea Department of Food Science and Nutrition Hallym University Chuncheon 200-702 Korea Silver Biotechnology Research Center Hallym University Chuncheon 200-702 Korea Korea Food Research Institute Songnam 463-746 Korea

AIM： To examine whether trans-10,cis-12 CLA （t10C12） or cis-9,trans-11 CLA （c9t11） inhibits heregulin （HRG）-β- stimulated cell growth and HRG-β-ErbB3 signaling in HT-29 cells. METHODS： We cultured HT-29 cells in the absence or presence of the CLA isomers and/or the ErbB3 ligand HRG-β. MTT assay, [^3H]thymidine incorporation, Annexin V staining, RT-PCR, Western blotting, immunoprecipitation, and in vitro kinase assay were performed. RESULTS： HRG-β increased cell growth, but did not prevent DNA t10c12-induced growth inhibition. T10C12 inhibited DNA synthesis and induced apoptosis of HT-29 cells, whereas c9t11 had no effect. T10c12 decreased the levels of ErbB1, ErbB2, and ErbB3 proteins and transcripts in a dose-dependent manner, whereas c9t11 had no effect. Immunoprecipitation/ Western blot studies revealed that t10c12 inhibited HRG- β-stimulated phosphorylation of ErbB3, recruitment of the p85 subunit of phosphoinositide 3-kinase （PI3K） to ErbB3, ErbB3-associated PI3K activities, and phosphorylation of Akt. However, c9t11 had no effect on phospho Aid： levels. Neither t10c12 nor c9t11 had any effect on HRG-β-induced phosphorylation of ERK-1/2. CONCLUSION： These results indicate that the inhibition of HT-29 cell growth by t10c12 may be induced via its modulation of ErbB3 signaling leading to inhibition of Akt activation.

关键词： Akt phosphoinositide 3-kinase DNA synthesis Apoptosis ERK-1/2

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Involvement of PI3K and ERK1/2 pathways in hepatocyte growth factor-induced cholangiocarcinoma cell invasion

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World Journal of Gastroenterology 2010年第6期16卷 713-722页

作者： Apaporn Menakongka Tuangporn Suthiphongchai Department of Biochemistry Faculty of ScienceMahidol University

AIM:To investigate the role of hepatocyte growth factor(HGF) in cholangiocarcinoma(CCA) cell invasiveness and the mechanisms underlying such cellular responses. METHODS:Effects of HGF on cell invasion and motility were investigated in two human CCA cell lines,HuCCA-1 and KKU-M213,using Transwell in vitro *** of proteins of interest and their phosphorylated forms were determined by Western *** of E-cadherin was analyzed by immunofluorescence staining and visualized under confocal microscope. Activities of matrix degrading enzymes were determined by zymography. RESULTS:Both CCA cell lines expressed higher Met levels than the H69 immortalized cholangiocyte cell *** induced invasion and motility of the cell lines and altered E-cadherin from membrane to cytoplasm localization,but did not affect the levels of secreted matrix metalloproteinase(MMP) -2,MMP-9 andurokinase plasminogen activator,key matrix degrading enzymes involved in cell ***,HGF stimulated Akt and extracellular signal-regulated kinase(ERK) 1/2 phosphorylation but with slightly different kinetic profiles in the two cell *** of the phosphoinositide 3-kinase(PI3K) /Akt pathway by the PI3K inhibitor,LY294002,markedly suppressed HGFstimulated invasion of both CCA cell lines,and inhibition of the ERK pathway by U0126 suppressed HGF-induced invasion of the KKU-M213 cell line but had a moderate effect on HuCCA-1 cells. CONCLUSION:These data indicate that HGF promotes CCA cell invasiveness through dys-localization of E-cadherin and induction of cell motility by distinct signaling pathways depending on cell line type.

关键词： Hepatocyte growth factor Invasion Cholangiocarcinoma phosphoinositide 3-kinase Extracellular signal-regulated kinase

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Dopamine and cyclic adenosine monophosphate-regulated phosphoprotein with an apparent Mr of 32000 promotes colorectal cancer growth

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World Journal of Gastrointestinal Oncology 2023年第11期15卷 1936-1950页

作者： Kuan He Chao-Zheng Xie Ya Li Zhen-Zhou Chen Shi-Hao Xu Si-Qi Huang Jian-Guo Yang Zheng-QiangWei Xu-Dong Peng Gastrointestinal Surgery The First Affiliated Hospital of Chongqing Medical UniversityChongqing 400000China Gastrointestinal Surgery The Third Affiliated Hospital of Chongqing Medical UniversityChongqing 400000China

BACKGROUND Dopamine and cyclic adenosine monophosphate(cAMP)-regulated phosphop-rotein with an apparent Mr of 32000(DARPP-32)is a protein that is involved in regulating dopamine and cAMP signaling pathways in the ***,recent studies have shown that DARPP-32 is also expressed in other tissues,including colorectal cancer(CRC),where its function is not well *** To explore the effect of DARPP-32 on CRC *** The expression levels of DARPP-32 were assessed in CRC tissues using both quantitative polymerase chain reaction and immunohistochemistry *** proliferative capacity of CRC cell lines was evaluated with Cell Counting Kit-8 and 5-ethynyl-2’-deoxyuridine assays,while apoptosis was measured by flow *** migratory and invasive potential of CRC cell lines were deter-mined using wound healing and transwell chamber *** vivo studies involved monitoring the growth rate of xenograft ***,the underlying molecular mechanism of DARPP-32 was investigated through RNA-sequencing and western blot *** DARPP-32 was frequently upregulated in CRC and associated with abnormal clinicopathological features in *** of DARPP-32 was shown to promote cancer cell proliferation,migration,and invasion and reduce ***-32 knockdown resulted in the opposite functional ***,DARPP-32 may regulate the phosphoinositide 3-kinase(PI3K)/AKT signaling pathway in order to carry out its biological *** DARPP-32 promotes CRC progression via the PI3K/AKT signaling pathway.

关键词： Colorectal cancer Dopamine and cyclic adenosine monophosphate-regulated phosphoprotein with an apparent Mr of 32000 Proliferation Migration phosphoinositide 3-kinase Akt

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GABAB receptor activation protects neurons from apoptosis via IGF-I receptor transactivation

GABAB receptor activation protects neurons from apoptosis vi...

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中国神经科学学会第四次会员代表大会暨第八届全国学术会议

作者： Philippe Rondard Jean-Philippe Pin Centre National de la Recherche Scientifique（CNRS） Unite Mixte de Recherche 5203Institut de Genomique FonctionnelleMontpellierFrance and INSERMU661MontpellierFrance and Universite Montpellier 12Montpellier F-34000France

＜正＞The G-protein coupled receptors（GPCRs） and receptor tyrosine kinases（RTKs） play key roles in cell-cell *** studies have revealed important synergisms between these two types of receptors,with some of the actions of either receptor being mediated through transactivation of the *** the large GPCR family,GABAB receptor is activated by the neurotransmitterγ-aminobutyric acid,and is expressed in most neurons where it mediates slow and prolonged inhibition of synaptic *** we show that this receptor is involved in the regulation of life and death decisions of cerebellar granule neurons（CGNs）.We show that specific activation of GABAB receptor can protect neurons from apoptosis through a mechanism that involves transactivation of the IGF-1 *** work demonstrated that this cross-talk was dependent on Gi/o-protein,PLC and PKC,while IGF-1 receptor-induced signaling involved Src kinase,PI3 kinase and Akt *** results reveal a new function for this important GPCR and further highlight the importance of functional cross-talk networks between GPCRs and *** results reveal GABAB receptor as a potential drug target for the treatment of neurodegenerative disorders.

关键词： GABAB receptor Baclofen apoptosis cerebellum neuroprotection phosphoinositide 3-kinase

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let-7d-5p/COL1A2调控轴对胃癌生物学行为的影响及其机制研究

let-7d-5p/COL1A2调控轴对胃癌生物学行为的影响及其机制研究

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作者：张剑锋中国医科大学

学位级别：硕士

目的:虽然全球范围内的胃癌的发生率和死亡率在逐步下降,但胃癌仍然是全球范围内最为常见的消化系统的恶性肿瘤之一。近年来,新辅助放化疗、手术治疗、术后放化疗及靶向治疗等联合性治疗的方法,在逐渐提高胃癌生存率的同时,可在一定程... 详细信息

目的:虽然全球范围内的胃癌的发生率和死亡率在逐步下降,但胃癌仍然是全球范围内最为常见的消化系统的恶性肿瘤之一。近年来,新辅助放化疗、手术治疗、术后放化疗及靶向治疗等联合性治疗的方法,在逐渐提高胃癌生存率的同时,可在一定程度上降低胃癌复发、转移的风险。然而胃癌起病隐匿、早期检出率低,且进展迅速,导致其治疗时病期较晚,很大程度上限制其治疗方式的选择和最终治疗效果。因此寻求有效的诊断和治疗的关键因子及其相关机制是改善胃癌预后的重要途径。近年来靶向治疗的研究,为胃癌患者提供了新的治疗思路。更加全面地了解胃癌的发生发展转移的内在机制,从而探寻更为有效的治疗靶点就显得尤为重要。方法:1.首先从GEO数据库中检索选取三组胃癌相关的芯片,利用R语言分别对每个芯片中所含基因进行差异分析,进而利用维恩图求出三组差异表达基因(DEGs)交集作为下一步研究对象。随后利用DAVID进行差异基因的GO/KEGG聚类分析,通过STRING进行蛋白互作网络分析,利用Cytoscape＿v3.9.0软件对蛋白互作网络进行进一步可视化处理获得核心基因(Hub gene)。通过GEPIA数据库验证Hub gene中各m RNA的表达情况;采用Kaplan-Meier plotter探究该部分基因对胃癌预后的影响,选择最终确定的研究靶基因:COL1A2。通过生物信息学分析进一步预测可能调控其表达的上游mi RNA(let-7d-5p)及其对下游可能通路的调节机制(PI3K-Akt信号通路)。***-7d-5p/COL1A2调控轴在胃癌中的表达及作用机制:收集于中国医科大学附属第一医院肿瘤外科因原发性胃癌行手术切除患者的胃癌组织及癌旁组织行免疫组化分析,研究COL1A2在胃癌组织和癌旁正常组织中的表达高低及其与患者临床病理特征及生存预后之间的关系。收集新鲜标本(胃癌组织和癌旁组织)做Western blotting分析,探究COL1A2在胃癌组织和癌旁正常组织中的表达差异。检测let-7d-5p在不同胃癌细胞系中的表达,选择合适的研究细胞系;双荧光素酶报告基因实验验证let-7d-5p是否可通过靶向结合COL1A2 m RNA的3’UTR而直接调控该蛋白;分别转染COL1A2过表达质粒和let-7d-5p过表达质粒,通过CCK-8试验、Matrigel胶粘附试验、划痕实验和Transwell试验分别验证COL1A2、let-7d-5p高表达时对于胃癌细胞的增殖、粘附、迁移、侵袭等生物学行为的影响;同时通过Western blotting实验探究COL1A2下游相关通路蛋白(PI3K、pPI3K、Akt、p-Akt)表达情况,从而验证该蛋白下游可能的调控通路。结果:1.在利用维恩图对芯片GSE79973、GSE54129和GSE118916差异基因分析后,共568个基因被证实为共同差异表达基因(|log FC|>1,p3K-Akt信号通路相关;2.经STRING与Cytoscape＿3.9.0分析后,有28个hub基因组成的分子网络相关性最强,利用GEPIA、Kaplan-Meier plotter工具验证其在胃癌中的表达及其与预后的关系,其中COL基因簇含量较高,而COL1A2在胃癌中的表达与调控有待进一步研究,因此我们选择COL1A2作为研究靶点;3.通过查阅文献及相关的生信分析,预测let-7d-5p可作为上游mi RNA调控COL1A2的表达,继而通过PI3K-Akt信号通路影响胃癌的增殖、迁移、粘附、侵袭等生物学行为。4.临床患者样本的免疫组化和Western blotting实验均提示COL1A2在胃癌组织中呈高表达,并与患者的肿瘤浸润深度(p=0.028)、淋巴结转移状态(P=0.004)、TNM分期(P=0.001)显著相关;生存分析提示,COL1A2高表达患者的预后较差(Log rank P3K和p-Akt表达明显增强,而let-7d-5p过表达时二者表达显著降低。结论:***1A2是胃癌中潜在的标记基因,其表达水平与胃癌生物学行为相关;***1A2在胃癌中呈高表达,且与

关键词：胃癌生物信息学 COL1A2 let-7d-5p phosphoinositide 3-kinase Akt

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