Suppr超能文献

自噬是抗癌药物耐药性中的一个治疗靶点。

Autophagy is a therapeutic target in anticancer drug resistance.

作者信息

Chen Suning, Rehman Sumaiyah K, Zhang Wei, Wen Aidong, Yao Libo, Zhang Jian

机构信息

Department of Pharmacy, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi Province 710032, People's Republic of China.

出版信息

Biochim Biophys Acta. 2010 Dec;1806(2):220-9. doi: 10.1016/j.bbcan.2010.07.003. Epub 2010 Jul 13.

Abstract

Autophagy is a type of cellular catabolic degradation response to nutrient starvation or metabolic stress. The main function of autophagy is to maintain intracellular metabolic homeostasis through degradation of unfolded or aggregated proteins and organelles. Although autophagic regulation is a complicated process, solid evidence demonstrates that the PI3K-Akt-mTOR, LKB1-AMPK-mTOR and p53 are the main upstream regulators of the autophagic pathway. Currently, there is a bulk of data indicating the important function of autophagy in cancer. It is noteworthy that autophagy facilitates the cancer cells' resistance to chemotherapy and radiation treatment. The abrogation of autophagy potentiates the re-sensitization of therapeutic resistant cancer cells to the anticancer treatment via autophagy inhibitors, such as 3-MA, CQ and BA, or knockdown of the autophagy related molecules. In this review, we summarize the accumulation of evidence for autophagy's involvement in mediating resistance of cancer cells to anticancer therapy and suggest that autophagy might be a potential therapeutic target in anticancer drug resistance in the future.

摘要

自噬是细胞对营养饥饿或代谢应激的一种分解代谢降解反应。自噬的主要功能是通过降解未折叠或聚集的蛋白质及细胞器来维持细胞内代谢稳态。尽管自噬调节是一个复杂的过程,但确凿证据表明,PI3K-Akt-mTOR、LKB1-AMPK-mTOR和p53是自噬途径的主要上游调节因子。目前,大量数据表明自噬在癌症中具有重要作用。值得注意的是,自噬促进癌细胞对化疗和放疗的抗性。通过自噬抑制剂(如3-MA、CQ和BA)或敲低自噬相关分子来消除自噬,可增强治疗抗性癌细胞对抗癌治疗的再敏化。在本综述中,我们总结了自噬参与介导癌细胞对抗癌治疗抗性的证据积累,并表明自噬可能是未来抗癌药物抗性的一个潜在治疗靶点。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验