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缺氧诱导因子(HIF)与原癌基因c-Myc:争夺癌细胞代谢与增殖控制权的“同胞对手”

HIF and c-Myc: sibling rivals for control of cancer cell metabolism and proliferation.

作者信息

Gordan John D, Thompson Craig B, Simon M Celeste

机构信息

Abramson Family Cancer Research Institute, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.

出版信息

Cancer Cell. 2007 Aug;12(2):108-13. doi: 10.1016/j.ccr.2007.07.006.

Abstract

O(2) deprivation (hypoxia) and cellular proliferation engage opposite cellular pathways, yet often coexist during tumor growth. The ability of cells to grow during hypoxia results in part from crosstalk between hypoxia-inducible factors (HIFs) and the proto-oncogene c-Myc. Acting alone, HIF and c-Myc partially regulate complex adaptations undertaken by tumor cells growing in low O(2). However, acting in concert these transcription factors reprogram metabolism, protein synthesis, and cell cycle progression, to "fine tune" adaptive responses to hypoxic environments.

摘要

氧(O₂)剥夺(缺氧)与细胞增殖涉及相反的细胞途径,但在肿瘤生长过程中却常常同时存在。细胞在缺氧条件下生长的能力部分源于缺氧诱导因子(HIFs)与原癌基因c-Myc之间的相互作用。单独作用时,HIF和c-Myc部分调节低氧环境中生长的肿瘤细胞所进行的复杂适应过程。然而,这些转录因子协同作用时会重新编程代谢、蛋白质合成和细胞周期进程,以“微调”对缺氧环境的适应性反应。

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