Graduate School of Humanity-Oriented Science and Engineering, Kindai University, Fukuoka, Japan
Department of Biological and Environmental Chemistry, Faculty of Humanity-Oriented Science and Engineering, Kindai University, Fukuoka, Japan.
Cancer Genomics Proteomics. 2020 Jul-Aug;17(4):425-430. doi: 10.21873/cgp.20201.
BACKGROUND/AIM: The INK4 locus encodes three important genes p15, p16, and ARF, which function to suppress oncogenesis, and a long noncoding RNA, ANRIL, which, in contrast, functions to promote oncogenesis. Herein, we report a fifth genetic element on the INK4 locus, a long noncoding RNA with unknown function named associated negative regulation of cell proliferation (ANROC), which played a role in the suppression of cell proliferation.
Following ANROC silencing in cells by siRNA, quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and cell cycle analysis using flow cytometry were performed.
ANROC expression was decreased by oncogenic RAS signalling. ANROC knockdown enhanced HeLa cell proliferation and induced cyclin B1 mRNA, which promotes G2/M progression of the cell cycle. Furthermore, flow cytometric analysis revealed that ANROC knockdown increased the percentage of cells in the S and G/M phases of the cell cycle.
ANROC functions to suppress cell cycle progression by suppressing cyclin B1 expression, thus inhibiting cell proliferation.
背景/目的:INK4 基因座编码三个重要基因 p15、p16 和 ARF,它们具有抑制致癌作用,而长链非编码 RNA ANRIL 则具有促进致癌作用。在此,我们报告 INK4 基因座上的第五个遗传元件,一个具有未知功能的长链非编码 RNA,命名为细胞增殖负调控相关(associated negative regulation of cell proliferation,ANROC),其在抑制细胞增殖中发挥作用。
用 siRNA 沉默细胞中的 ANROC 后,进行定量逆转录聚合酶链反应(qRT-PCR)和流式细胞术细胞周期分析。
致癌性 RAS 信号降低了 ANROC 的表达。ANROC 敲低增强了 HeLa 细胞的增殖,并诱导了促进细胞周期 G2/M 进程的细胞周期蛋白 B1 mRNA。此外,流式细胞术分析显示,ANROC 敲低增加了细胞周期 S 和 G/M 期的细胞百分比。
ANROC 通过抑制细胞周期蛋白 B1 的表达来抑制细胞周期的进展,从而抑制细胞增殖。