当前位置:主页 > 医学论文 > 泌尿论文 >

自噬在前列腺癌的研究进展

发布时间:2018-07-25 07:38
【摘要】:自噬是一个基因编程、进化保守的过程,通过对过多的、有害的,或衰老的蛋白质和细胞器进行降解,保持对重要细胞成分的控制,在正常生物体内扮演着重要角色。研究发现,自噬与肿瘤关系密切,对肿瘤发生和发展起着重要作用。在前列腺癌细胞中,自噬的发生不仅对前列腺癌的进展转移有着重要促进作用,而且还能通过保护前列腺癌细胞免受外界环境变化的影响,对治疗前列腺癌的药物产生抵抗。自噬可通过多种蛋白酶、细胞因子及基因包括腺苷酸活化蛋白酶、单核细胞趋化蛋白1、酪氨酸激酶、mda-7/IL-24及P21等的调控参与对前列腺癌产生影响,而运用异戊烯半胱氨酸羧甲基转移酶抑制剂、非瑟酮、二甲双胍与2脱氧葡萄糖等药物来抑制自噬可诱导前列腺癌凋亡。因此,探讨自噬在前列腺癌中的调控机理,开发相关的自噬抑制药物,可为前列腺癌的治疗提供新方法。
[Abstract]:Autophagy is a genetically programmed, evolutionarily conserved process that plays an important role in normal organisms by degrading excessive, harmful, or aging proteins and organelles and maintaining control over important cellular components. It has been found that autophagy is closely related to tumor and plays an important role in tumorigenesis and development. In prostate cancer cells autophagy not only plays an important role in promoting the progression and metastasis of prostate cancer but also can protect prostate cancer cells from the effects of environmental changes. Autophagy plays an important role in prostate cancer through the regulation of a variety of proteases, cytokines and genes, including adenylate activated protease, monocyte chemoattractant protein 1, tyrosine kinase mda-7 / IL-24 and P21, etc. Inhibition of autophagy by isopentene cysteine carboxymethyl transferase inhibitor, fenestrone, metformin and 2 deoxyglucose could induce apoptosis of prostate cancer. Therefore, to explore the regulatory mechanism of autophagy in prostate cancer and to develop related autophagy inhibitors may provide a new method for the treatment of prostate cancer.
【学位授予单位】:重庆医科大学
【学位级别】:硕士
【学位授予年份】:2014
【分类号】:R737.25

【参考文献】

相关期刊论文 前1条

1 Gy銉rgyi M,

本文编号:2143103


资料下载
论文发表

本文链接:https://www.wllwen.com/yixuelunwen/mjlw/2143103.html


Copyright(c)文论论文网All Rights Reserved | 网站地图 |

版权申明:资料由用户13520***提供,本站仅收录摘要或目录,作者需要删除请E-mail邮箱bigeng88@qq.com