Tianjin Life Science Research Center and Basic Medical School, Tianjin Medical University, Tianjin, China.
Cancer Lett. 2013 Jul 28;335(2):351-60. doi: 10.1016/j.canlet.2013.02.045. Epub 2013 Mar 4.
Increasing evidence has lent support to the notion that miRNAs regulate hepatocellular carcinoma (HCC) cell proliferation by directly targeting cell cycle-related genes. Among these genes, we identified PRPF4B, a CDK-like kinase, as a new target of miR-371-5p. Over-expression of miR-371-5p and knockdown of PRPF4B promotes cell growth by accelerating the G1/S transition in HCC cell lines. Moreover, miR-371-5p promotes tumor growth of QGY-7703 cells in vivo. Conversely, inhibition of miR-371-5p yields an opposing effect. Ectopic expression of PFPF4B abolishes the malignant phenotypes caused by miR-371-5p. Furthermore, contrary to PRPF4B, miR-371 was up-regulated in HCC tissues. Collectively, we highlight the significance of miR-371-5p and PRPF4B in cell cycle progression and hepatocarcinogenesis.
越来越多的证据支持这样一种观点,即 miRNAs 通过直接靶向细胞周期相关基因来调节肝细胞癌 (HCC) 细胞的增殖。在这些基因中,我们鉴定出 PRPF4B(一种 CDK 样激酶)是 miR-371-5p 的一个新靶点。miR-371-5p 的过表达和 PRPF4B 的敲低通过加速 HCC 细胞系中的 G1/S 转换促进细胞生长。此外,miR-371-5p 在体内促进 QGY-7703 细胞的肿瘤生长。相反,抑制 miR-371-5p 则产生相反的效果。过表达 PFPF4B 可消除 miR-371-5p 引起的恶性表型。此外,与 PRPF4B 相反,miR-371 在 HCC 组织中上调。总的来说,我们强调了 miR-371-5p 和 PRPF4B 在细胞周期进展和肝癌发生中的重要性。