Graduate School of Humanity-Oriented Science and Engineering, Kindai University, Fukuoka, Japan.
Department of Otorhinolaryngology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Anticancer Res. 2019 Aug;39(8):4073-4077. doi: 10.21873/anticanres.13564.
BACKGROUND/AIM: ANRIL is a long noncoding RNA located on INK4 locus, which encodes p15 and p16 that cause G phase arrest in the cell cycle. ANRIL positively regulates proliferation of several kinds of cancer cells such as lung and gastric cancers. This study, examined the effect of ANRIL in head and neck squamous cell carcinoma cells.
Cells were transfected with siRNA oligonucleotides targeting ANRIL. Transfected cells were subjected to cell-cycle and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analysis.
Depletion of ANRIL increased p15 mRNA in FaDu cells, and p15 and p16 mRNA in CAL27 cells and inhibited proliferation of these cells. Cell cycle analysis showed that depletion of ANRIL caused arrest at the G phase of the cell cycle.
ANRIL promotes G phase progression by repressing p15 and p16, and thus promotes FaDu and CAL27 cell proliferation.
背景/目的:ANRIL 是位于 INK4 基因座上的长链非编码 RNA,它编码 p15 和 p16,导致细胞周期的 G 期停滞。ANRIL 正向调节多种癌细胞的增殖,如肺癌和胃癌。本研究探讨了 ANRIL 在头颈部鳞状细胞癌细胞中的作用。
用靶向 ANRIL 的 siRNA 寡核苷酸转染细胞。转染后的细胞进行细胞周期和定量逆转录聚合酶链反应(qRT-PCR)分析。
在 FaDu 细胞中,ANRIL 的缺失增加了 p15 mRNA,在 CAL27 细胞中增加了 p15 和 p16 mRNA,并抑制了这些细胞的增殖。细胞周期分析表明,ANRIL 的缺失导致细胞周期的 G 期停滞。
ANRIL 通过抑制 p15 和 p16 促进 G 期进展,从而促进 FaDu 和 CAL27 细胞的增殖。