Mitogen-activated protein kinase kinase 3 induces cell cycle arrest via p38 activation mediated Bmi-1 downregulation in hepatocellular carcinoma

作者: LIN WANG , CHEN CHEN , SHUZHI FENG , PING LEI , JIANLI TIAN

DOI: 10.3892/MMR.2015.4564

关键词:

摘要: The underlying molecular pathogenesis of hepatocellular carcinoma (HCC) remains poorly understood. Mitogen-activated protein kinase 3 (MKK3), has been reported as a novel tumor suppressor in breast cancer. However, its potential suppressive role HCC not evaluated. In the current study, biologic functions MKK3 were investigated and previously unreported cell cycle regulation mechanism was observed. overexpression suppressed HepG2 PLC‑PRF‑5 proliferation induced arrest two lines. addition, upregulated cyclin-dependent inhibitors, p16 INK4A p15 INK4B cells. Their negative regulator, Bim‑1, downregulated following overexpression. Moreover, activated p38 cells SB203580, inhibitor, reversed effect MKK3. conclusion, results identify highlighted significance pathway aberration HCC.

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