Naemura Madoka, Murasaki Chihiro, Inoue Yasutoshi, Okamoto Haruna, Kotake Yojiro
Department of Biological and Environmental Chemistry, Faculty of Humanity-Oriented Science and Engineering, Kinki University, Fukuoka, Japan.
Department of Biological and Environmental Chemistry, Faculty of Humanity-Oriented Science and Engineering, Kinki University, Fukuoka, Japan
Anticancer Res. 2015 Oct;35(10):5377-82.
Long noncoding RNA ANRIL (antisense non-coding RNA in the INK4 locus) represses p15 and p16, which induce cell-cycle arrest at G1 phase, leading to enhanced cell proliferation of normal fibroblasts. Herein we report that ANRIL is also involved in the regulation of cancer-cell proliferation.
HeLa and H1299 cells were transfected with ANRIL siRNAs. At 72 h post-transfection, cells were subjected to quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and cell-cycle analysis.
qRT-PCR showed that ANRIL is highly expressed in these cancer cells compared to normal fibroblasts. Depletion of ANRIL increased p15 expression, with no impact on p16 or ARF (alternative reading frame) expression, and caused cell-cycle arrest at the G2/M phase, leading to inhibition of proliferation of H1299 and HeLa cells.
ANRIL positively regulates the proliferation of cancer cells, such as H1299 and HeLa cells, via regulating p15 and other genes related to G2/M phase control.
长链非编码RNA ANRIL（INK4基因座中的反义非编码RNA）可抑制p15和p16，这两种蛋白可诱导细胞周期在G1期停滞，从而导致正常成纤维细胞的细胞增殖增强。在此我们报告ANRIL也参与癌细胞增殖的调控。
用ANRIL小干扰RNA转染HeLa和H1299细胞。转染后72小时，对细胞进行定量逆转录-聚合酶链反应（qRT-PCR）和细胞周期分析。
qRT-PCR显示，与正常成纤维细胞相比，ANRIL在这些癌细胞中高表达。敲低ANRIL可增加p15表达，对p16或ARF（可变阅读框）表达无影响，并导致细胞周期在G2/M期停滞，从而抑制H1299和HeLa细胞的增殖。
ANRIL通过调控p15及其他与G2/M期调控相关的基因，正向调节H1299和HeLa等癌细胞的增殖。
