Mao Weidong, Guo Ziyang, Dai Yingchu, Nie Jing, Li Bingyan, Pei Hailong, Zhou Guangming
State Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou 215123, China.
The Second Affiliated Hospital of Soochow University, Suzhou 215123, China.
J Cancer. 2019 Jun 2;10(12):2764-2770. doi: 10.7150/jca.31703. eCollection 2019.
Long noncoding RNAs (lncRNAs) are usually associated with tumor development and progression and some of them are dysregulated in various human cancers. The mechanisms underlying their dysregulation are worth further study. Here, we demonstrate that the expression level of LNC CRYBG3 is correlated with 1501 aberrantly expressed proteins in A549 cells (non-small cell lung cancer (NSCLC) cells). LNC CRYBG3 overexpression results in M phase arrest and promoted cell death, whereas LNC CRYBG3 knockdown did not elicit the opposite effects. The overexpression of LNC CRYBG3 inhibits cell proliferation both and in vivo. Moreover, it upregulates the expression of cyclin B1 and the phosphorylation of H3, whereas it inhibited the expression of cyclin-dependent kinase 6 and cyclin D1. Taken together, these findings suggest that LNC CRYBG3 regulates the cell cycle process of A549 cells, suggesting its potential application for the treatment of this disease.
长链非编码RNA(lncRNAs)通常与肿瘤的发生和发展相关,其中一些在多种人类癌症中表达失调。其表达失调的潜在机制值得进一步研究。在此,我们证明LNC CRYBG3的表达水平与A549细胞(非小细胞肺癌(NSCLC)细胞)中1501种异常表达的蛋白质相关。LNC CRYBG3的过表达导致M期阻滞并促进细胞死亡,而LNC CRYBG3的敲低并未产生相反的效果。LNC CRYBG3的过表达在体内和体外均抑制细胞增殖。此外,它上调细胞周期蛋白B1的表达和H3的磷酸化,而抑制细胞周期蛋白依赖性激酶6和细胞周期蛋白D1的表达。综上所述,这些发现表明LNC CRYBG3调节A549细胞的细胞周期进程,提示其在该疾病治疗中的潜在应用价值。