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HIF-1 regulates mitochondrial function in bone marrow-derived macrophages but not in tissue-resident alveolar macrophages.低氧诱导因子-1(HIF-1)调节骨髓源性巨噬细胞的线粒体功能,但不调节组织驻留肺泡巨噬细胞的线粒体功能。
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本文引用的文献

1
HIF-1 inhibits mitochondrial biogenesis and cellular respiration in VHL-deficient renal cell carcinoma by repression of C-MYC activity.缺氧诱导因子-1通过抑制C-MYC活性来抑制VHL基因缺陷型肾细胞癌中的线粒体生物发生和细胞呼吸。
Cancer Cell. 2007 May;11(5):407-20. doi: 10.1016/j.ccr.2007.04.001.
2
The transcription factor HIF-1alpha plays a critical role in the growth factor-dependent regulation of both aerobic and anaerobic glycolysis.转录因子缺氧诱导因子-1α(HIF-1α)在生长因子依赖性的有氧糖酵解和无氧糖酵解调节中发挥关键作用。
Genes Dev. 2007 May 1;21(9):1037-49. doi: 10.1101/gad.1529107. Epub 2007 Apr 16.
3
HIF-1 regulates cytochrome oxidase subunits to optimize efficiency of respiration in hypoxic cells.缺氧诱导因子-1调节细胞色素氧化酶亚基,以优化缺氧细胞中的呼吸效率。
Cell. 2007 Apr 6;129(1):111-22. doi: 10.1016/j.cell.2007.01.047.
4
HIF-2alpha promotes hypoxic cell proliferation by enhancing c-myc transcriptional activity.缺氧诱导因子-2α通过增强c-myc转录活性促进缺氧细胞增殖。
Cancer Cell. 2007 Apr;11(4):335-47. doi: 10.1016/j.ccr.2007.02.006.
5
Intermittent hypoxia furthers the rationale for hypoxia-inducible factor-1 targeting.间歇性低氧进一步支持了靶向缺氧诱导因子-1的理论依据。
Cancer Res. 2007 Feb 1;67(3):854-5. doi: 10.1158/0008-5472.CAN-06-4744.
6
Recruitment of HIF-1alpha and HIF-2alpha to common target genes is differentially regulated in neuroblastoma: HIF-2alpha promotes an aggressive phenotype.在神经母细胞瘤中,低氧诱导因子-1α(HIF-1α)和低氧诱导因子-2α(HIF-2α)募集到共同靶基因的过程受到不同调控:HIF-2α促进侵袭性表型。
Cancer Cell. 2006 Nov;10(5):413-23. doi: 10.1016/j.ccr.2006.08.026.
7
The phosphorylation status of PAS-B distinguishes HIF-1alpha from HIF-2alpha in NBS1 repression.在NBS1抑制过程中,PAS-B的磷酸化状态可区分HIF-1α和HIF-2α。
EMBO J. 2006 Oct 18;25(20):4784-94. doi: 10.1038/sj.emboj.7601369. Epub 2006 Oct 5.
8
PML inhibits HIF-1alpha translation and neoangiogenesis through repression of mTOR.PML通过抑制mTOR来抑制HIF-1α的翻译和新生血管生成。
Nature. 2006 Aug 17;442(7104):779-85. doi: 10.1038/nature05029.
9
How do cancer cells acquire the fuel needed to support cell growth?癌细胞如何获取支持细胞生长所需的养分?
Cold Spring Harb Symp Quant Biol. 2005;70:357-62. doi: 10.1101/sqb.2005.70.011.
10
Attenuation of LDH-A expression uncovers a link between glycolysis, mitochondrial physiology, and tumor maintenance.乳酸脱氢酶A(LDH-A)表达的减弱揭示了糖酵解、线粒体生理学与肿瘤维持之间的联系。
Cancer Cell. 2006 Jun;9(6):425-34. doi: 10.1016/j.ccr.2006.04.023.

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.

DOI:10.1016/j.ccr.2007.07.006
PMID:17692803
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3215289/
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。