COLPH3、PI3K/Akt/mTOR信号通路与胃癌发生、发展关系
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摘要
胃癌的发生、发展过程较为复杂,在此过程中不但会涉及基因突变,还会涉及细胞中信传导通路改变。细胞中重要的一种信号传导通路为磷脂肌醇3-激酶(phosphoinositide-3 kinase,PI3K)/蛋白激酶B(protein kinase B,AKT)/哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)通路,参与了胃癌侵袭与转移过程,可对多种刺激作用诱发的机体胃癌细胞凋亡进行有效抑制,对血管的形成与细胞的周期进展产生促进作用。高尔基磷酸化蛋白-3(Golgi phosphoprotein-3,GOLPH3)基因及其表达产物在胃癌的发生、发展过程中起着重要作用,可促进肿瘤细胞的生长与增殖。本文主要对COLPH3、PI3K/Akt/mTOR信号通路与胃癌发生、发展关系进行探究,旨在为临床治疗提供有效的参考价值。
Gastric cancer occurrence,development process is relatively complicated,in the process not only involves gene mutations,also involves the citic pathway of cellular changes.A kind of important signaling pathways in cells for phospholipids 3-inositol kinase(phosphoinositide 3 kinase,PI3K)/egg white kinase B(protein kinase B,AKT)/mammals rapamycin target protein(mammalian target of rapamycin,mTOR) pathway,involved in gastric cancer invasion and metastasis process,and for a variety of stimulation induced body effectively inhibiting gastric cancer cell apoptosis,in the formation of blood vessels and cell cycle progression.Golgi protein phosphorylation-3(Golgi phosphoprotein,GOLPH3) gene and its expression in gastric cancer occurrence,development of the product plays an important role in the process,can promote the growth and proliferation of tumor cells.This article mainly discusses the COLPH3,PI3K/Akt/mTOR signaling pathway and explore the relationship between gastric cancer occurrence and development,to provide effective reference value for clinical treatment.
Gastric cancer occurrence,development process is relatively complicated,in the process not only involves gene mutations,also involves the citic pathway of cellular changes.A kind of important signaling pathways in cells for phospholipids 3-inositol kinase(phosphoinositide 3 kinase,PI3K)/egg white kinase B(protein kinase B,AKT)/mammals rapamycin target protein(mammalian target of rapamycin,mTOR) pathway,involved in gastric cancer invasion and metastasis process,and for a variety of stimulation induced body effectively inhibiting gastric cancer cell apoptosis,in the formation of blood vessels and cell cycle progression.Golgi protein phosphorylation-3(Golgi phosphoprotein,GOLPH3) gene and its expression in gastric cancer occurrence,development of the product plays an important role in the process,can promote the growth and proliferation of tumor cells.This article mainly discusses the COLPH3,PI3K/Akt/mTOR signaling pathway and explore the relationship between gastric cancer occurrence and development,to provide effective reference value for clinical treatment.
引文
[1]斯庆图娜拉,刘磊.抑制自噬增加PI3K/AKT/m TOR信号通路抑制剂引起的胃癌细胞死亡[J].中国实验诊断学,2015,19(9):1457-1460.
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[3]潘理会,张平,李春辉,等.PI3K/AKT/m TOR信号传导通路在胃癌中的研究进展[J].承德医学院学报,2016,33(4):324-327.
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[9]詹泽栩,韦尉元,曹稳珑,等.mi R-1284过表达对胃癌细胞中EIF4A1的影响[J].中国临床新医学,2016,9(2):97-101.
[10]刘慧,李鑫,胡腾鹏,等.PI3K/AKT/m TOR信号通路抑制剂在淋巴瘤中的研究进展[J].中国肿瘤临床,2016,43(5):211-215.
[11]Tapia O,Riquelme I,Leal P,et al.The PI3K/AKT/m TORpathway is activated in gastric cancer with potential prognostic and predictive significance[J].Virchows Archiv:an International Journal of Pathology,2014,465(1):25-33.
[12]张保豫,侯博,何海勇,等.内质网应激通过抑制PI3K/AKT/m TOR信号通路诱导多形性胶质母细胞瘤干细胞凋亡的机制[J].中山大学学报(医学科学版),2016,37(2):183-189.
[13]肖晨,苏东星,潘志刚,等.抑癌基因p16在疣状胃炎和胃癌中的表达及其意义[J].中国临床新医学,2011,4(4):303-305.
[14]周志平,郭延塔,余外市,等.高尔基磷酸化蛋白3在胃癌组织中的表达及其临床意义[J].中华实验外科杂志,2015,32(3):467-469.
[15]王梦阳,刘兴洲.PI3K/Akt/m TOR信号通路在FCDⅡb型发病机制中的作用[J].中华神经医学杂志,2014,13(4):415-417.
[16]柳望舒,俞松.PI3 K/AKt/m TOR信号通路与肿瘤关系的研究进展[J].实用医院临床杂志,2016,13(4):20-23.
[17]谢芳,赖铭裕,农云翠,等.沉默GOLPH3基因对胃癌细胞增殖、凋亡的影响及机制探讨[J].山东医药,2016,56(10):7-9.
[18]潘地铃,张声,王行富,等.CDH17表达及其SNPs在胃癌发生发展中的意义[J].中国肿瘤临床,2015,42(19):957-962.
[19]吴永勇.试析血管内皮抑素及碱性成纤维细胞生长因子在人胃癌组织中的表达[J].中国医学创新,2014,11(22):151-153.
[20]Cao Yubo,Qu Jinglei,Li Ce,et al.Celecoxib sensitizes gastric cancer to rapamycin via inhibition of the Cbl-b-regulated PI3K/Akt pathway[J].Tumour Biology:the Journal of the International Society for Onco Developmental Biology and Medicine,2015,36(7):5607-5615.
[21]梁君铭,曾宽,骆雪梅,等.胃癌患者VEGF及SSTR表达及与胃癌的相关性研究[J].中国医学创新,2015,12(28):35-37.
[22]叶石才,孙碧兰,黄昕,等.Eph受体酪氨酸激酶A2和CD133在胃癌组织的表达及其与胃癌发生发展的关系[J].中华实验外科杂志,2015,32(1):165-167.
[23]戎瑞洲,韩志伟,李曙晶,等.ZNF451和TGF-β在胃癌中的表达及其与临床病理特征及预后的相关性研究[J].中国医学创新,2016,13(23):1-5.
[24]周睿卿,龚玉萍,邢宏运,等.人胚胎干细胞Pten基因表达及PI3K/Akt/m TOR信号通路下游蛋白的磷酸化[J].中国组织工程研究与临床康复,2011,15(49):9207-9210.
[25]李建琦,陈敏,张松,等.PPIs抑制PI3K/Akt/m TOR信号通路逆转胃癌细胞的化疗多药耐药[J].胃肠病学,2012,17(10):579-586.
[26]滕玥,戴冬秋,沈文静,等.h MLH1基因启动子区甲基化在胃癌阶段性发生发展中的作用[J].中华胃肠外科杂志,2015,16(2):166-170.
[2]林贤东,胡丹,陈刚,等.PI3K-AKT-m TOR信号通路基因多态性与胃癌遗传易感相关性[J].临床与实验病理学杂志,2016,32(4):361-365,369.
[3]潘理会,张平,李春辉,等.PI3K/AKT/m TOR信号传导通路在胃癌中的研究进展[J].承德医学院学报,2016,33(4):324-327.
[4]程玉,李春辉.胃癌中Cx43与PI3K/Akt/m TOR信号通路相关性的研究进展[J].承德医学院学报,2013,30(5):419-422.
[5]Chen G,Chen S M,Wang X,et al.Inhibition of chemokine(CXC motif)ligand 12/chemokine(CXC motif)receptor 4axis(CXCL12/CXCR4)-mediated cell migration by targeting mammalian target of rapamycin(m TOR)pathway in human gastric carcinoma cells[J].The Journal of Biological Chemistry,2012,287(15):12 132-12 141.
[6]宿恒川,孙福康.PI3K/Akt/m TOR信号通路及m TOR抑制剂在泌尿系统肿瘤中的研究进展[J].上海交通大学学报(医学版),2012,32(5):674-678.
[7]张丹丹,李庆林.PI3K/Akt/m TOR信号通路与肿瘤[J].安徽医药,2012,16(3):281-283.
[8]Zhang C H,Awasthi N,Schwarz M A,et al.The dual PI3K/m TOR inhibitor NVP-BEZ235 enhances nab-paclitaxel antitumor response in experimental gastric cancer[J].International Journal of Oncology,2013,43(5):1627-1635.
[9]詹泽栩,韦尉元,曹稳珑,等.mi R-1284过表达对胃癌细胞中EIF4A1的影响[J].中国临床新医学,2016,9(2):97-101.
[10]刘慧,李鑫,胡腾鹏,等.PI3K/AKT/m TOR信号通路抑制剂在淋巴瘤中的研究进展[J].中国肿瘤临床,2016,43(5):211-215.
[11]Tapia O,Riquelme I,Leal P,et al.The PI3K/AKT/m TORpathway is activated in gastric cancer with potential prognostic and predictive significance[J].Virchows Archiv:an International Journal of Pathology,2014,465(1):25-33.
[12]张保豫,侯博,何海勇,等.内质网应激通过抑制PI3K/AKT/m TOR信号通路诱导多形性胶质母细胞瘤干细胞凋亡的机制[J].中山大学学报(医学科学版),2016,37(2):183-189.
[13]肖晨,苏东星,潘志刚,等.抑癌基因p16在疣状胃炎和胃癌中的表达及其意义[J].中国临床新医学,2011,4(4):303-305.
[14]周志平,郭延塔,余外市,等.高尔基磷酸化蛋白3在胃癌组织中的表达及其临床意义[J].中华实验外科杂志,2015,32(3):467-469.
[15]王梦阳,刘兴洲.PI3K/Akt/m TOR信号通路在FCDⅡb型发病机制中的作用[J].中华神经医学杂志,2014,13(4):415-417.
[16]柳望舒,俞松.PI3 K/AKt/m TOR信号通路与肿瘤关系的研究进展[J].实用医院临床杂志,2016,13(4):20-23.
[17]谢芳,赖铭裕,农云翠,等.沉默GOLPH3基因对胃癌细胞增殖、凋亡的影响及机制探讨[J].山东医药,2016,56(10):7-9.
[18]潘地铃,张声,王行富,等.CDH17表达及其SNPs在胃癌发生发展中的意义[J].中国肿瘤临床,2015,42(19):957-962.
[19]吴永勇.试析血管内皮抑素及碱性成纤维细胞生长因子在人胃癌组织中的表达[J].中国医学创新,2014,11(22):151-153.
[20]Cao Yubo,Qu Jinglei,Li Ce,et al.Celecoxib sensitizes gastric cancer to rapamycin via inhibition of the Cbl-b-regulated PI3K/Akt pathway[J].Tumour Biology:the Journal of the International Society for Onco Developmental Biology and Medicine,2015,36(7):5607-5615.
[21]梁君铭,曾宽,骆雪梅,等.胃癌患者VEGF及SSTR表达及与胃癌的相关性研究[J].中国医学创新,2015,12(28):35-37.
[22]叶石才,孙碧兰,黄昕,等.Eph受体酪氨酸激酶A2和CD133在胃癌组织的表达及其与胃癌发生发展的关系[J].中华实验外科杂志,2015,32(1):165-167.
[23]戎瑞洲,韩志伟,李曙晶,等.ZNF451和TGF-β在胃癌中的表达及其与临床病理特征及预后的相关性研究[J].中国医学创新,2016,13(23):1-5.
[24]周睿卿,龚玉萍,邢宏运,等.人胚胎干细胞Pten基因表达及PI3K/Akt/m TOR信号通路下游蛋白的磷酸化[J].中国组织工程研究与临床康复,2011,15(49):9207-9210.
[25]李建琦,陈敏,张松,等.PPIs抑制PI3K/Akt/m TOR信号通路逆转胃癌细胞的化疗多药耐药[J].胃肠病学,2012,17(10):579-586.
[26]滕玥,戴冬秋,沈文静,等.h MLH1基因启动子区甲基化在胃癌阶段性发生发展中的作用[J].中华胃肠外科杂志,2015,16(2):166-170.