期刊文献+

mTOR信号转导通路抑制剂及其与肿瘤耐药的研究进展 被引量:1

Research Progress of Inhibitors in mTOR Signal Transduction Pathway and Drug Resistance in Tumor
原文传递
导出
摘要 哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,mTOR)是一种特异性的蛋白激酶,在调控细胞生长、增殖、代谢等多项生命活动中都具有重要意义。mTOR调控功能的失活与异常激活,会导致相关肿瘤和疾病的发生。近年来已有多种mTOR抑制剂用于治疗该信号转导通路异常引起的肿瘤。该文探究多种调控mTOR的信号通路和mTOR抑制剂用于肿瘤治疗的最新进展,还探讨肿瘤细胞对mTOR抑制剂产生耐药性的潜在机制和应对策略。因此,对mTOR信号通路及其调控机制的探索有助于研发全新的肿瘤治疗技术。 mTOR(mammalian target of rapamycin)is an evolutionary protein kinase that senses multiple upstream stimuli to regulate cell growth,proliferation,metabolism and many other vital activities.The inactivation and abnormal activation of mTOR regulatory functions will lead to the occurrence of related tumors and diseases.In recent years,a variety of mTOR inhibitors have been used to treat tumors caused by abnormal regulation of this signaling transduction pathway.The latest advances in mTOR inhibitors for tumor treatment are listed,and the potential mechanisms by which tumor cells develop resistance to mTOR inhibitors are also explored.Therefore,in-depth study of the mTOR signal transduction pathway and its regulatory mechanism contributes to the development of new tumor treatment technologies.
作者 何超 刘楠 张瑞 唐景峰 HE Chao;LIU Nan;ZHANG Rui;TANG Jingfeng(Department of Biomedicine,School of Food and Biological Engineering,Hubei University of Technology,Wuhan 430068,China;National“111”Center for Cellular Regulation and Molecular Pharmaceutics,Hubei University of Technolo)
出处 《中国细胞生物学学报》 CAS CSCD 2023年第2期274-282,共9页 Chinese Journal of Cell Biology
基金 国家自然科学基金(批准号:32000523、32070726) 2020年省科技厅自然基金青年项目(批准号:2020CFB413)资助的课题。
关键词 mTOR信号转导通路 肿瘤 耐药性 靶向治疗 mTOR signal transduction pathway tumor drug resistance targeted therapy
  • 相关文献

参考文献2

二级参考文献44

  • 1Kim J, Kundu M, Viollet B, Guan KL. AMPK and mTOR regulate autophagy through direct phosphorylation of Ulkl. Nat Cell Biol 2011; 13:132-141.
  • 2Laplante M, Sabatini DM. mTOR signaling in growth control and disease. Cell 2012; 149:274-293.
  • 3Ben-Sahra I, Howell JJ, Asara JM, Manning BD. Stimulation of de novo pyrimidine synthesis by growth signaling through mTOR and S6K1. Science 2013; 339:1323-1328.
  • 4Robitaille AM, Christen S, Shimobayashi M, et al. Quantita- tive phosphoproteomics reveal mTORC1 activates de novo pyrimidine synthesis. Science 2013; 339:1320-1323.
  • 5Jacinto E, Loewith R, Schmidt A, et al. Mammalian TOR complex 2 controls the actin cytoskeleton and is rapamycin insensitive. Nat Cell Biol 2004; 6: 1122-1128.
  • 6Sarbassov DD, Oucrtin DA, Ali SM, Sabatini DM. Phosphor- ylation and regulation of Akt/PKB by thc dctor-mTOR cam- plex. Science 2005; 307: 1098-1101.
  • 7Sarbasqov DD, Ali SM, Sengupta S, et al. Prolonged rapamy- cin treatment inhibits mTORC2 assembly and Akt/PKB. Mol Cell 2006; 22:150-168.
  • 8(iarcia-Martincz J M, Alessi DR. roTOR complex 2 (mTORC2) controla hydrophobic motif phosphorylation and activation of serum- and glueocorticoid-indueed protein kinase 1 (SGK1). Riochem J 2008; 416:375-385.
  • 9Guertin DA, ,qtcvcns DM, Thorcen CC, et al. Ablation in mice of the mTORC componcnts raptor, rictor, or mLST8 rcveals that mTORC2 is required for sip, haling to Akt-FOXO and PKCalpha, but not S6K 1. Dev Cell 2006; 11:859-871.
  • 10Dibble CC, Asara JM, Manning BD. Characterization of Ric- tor phosphorylation sites reveals direct regulation of roTOR complex 2 by S6K 1. Mol Cell Biol 2009; 29:5657-5670.

共引文献26

同被引文献5

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部