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丙酮酸激酶 M2 通过调节 Bcl-xL 的转录水平促进胃癌细胞的生长。

Pyruvate kinase M2 promotes the growth of gastric cancer cells via regulation of Bcl-xL expression at transcriptional level.

机构信息

Medical Genomics Research Center, KRIBB, Daejeon 305-806, Republic of Korea.

出版信息

Biochem Biophys Res Commun. 2012 Jun 22;423(1):38-44. doi: 10.1016/j.bbrc.2012.05.063. Epub 2012 May 22.

DOI:10.1016/j.bbrc.2012.05.063
PMID:22627140
Abstract

PKM2 is an isoenzyme of the glycolytic enzyme pyruvate kinase that promotes aerobic glycolysis. Here, we describe an important role for PKM2 in regulating the survival of gastric cancer (GC) cells. We showed that PKM2 was overexpressed in gastric tumor tissues compared to normal tissues and its expression level was associated with poor survival of gastric cancer patients. We also showed that PKM2 affected cell survival by regulating Bcl-xL at the transcriptional level. PKM2 knockdown partially affected the stability of NF-kB subunit p65, suggesting that post-translational regulation of p65 by PKM2 is one of plausible mechanisms for the increased cell growth. Therefore, PKM2 may function as an upstream molecule that regulates p65 function and thus enhances the growth of tumor cells.

摘要

PKM2 是糖酵解酶丙酮酸激酶的同工酶,能促进有氧糖酵解。在这里,我们描述了 PKM2 在调节胃癌(GC)细胞存活中的重要作用。我们发现与正常组织相比,PKM2 在胃癌肿瘤组织中过度表达,其表达水平与胃癌患者的不良预后相关。我们还发现 PKM2 通过转录水平调节 Bcl-xL 影响细胞存活。PKM2 敲低部分影响 NF-κB 亚基 p65 的稳定性,提示 PKM2 对 p65 的翻译后调节可能是其增加细胞生长的一种合理机制。因此,PKM2 可能作为一种上游分子调节 p65 的功能,从而增强肿瘤细胞的生长。

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