LNC CRYBG3 inhibits tumor growth by inducing M phase arrest
LNC CRYBG3 inhibits tumor growth by inducing M phase arrest
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LNC CRYBG3 通过诱导 M 期阻滞抑制肿瘤生长
DOI：
10.7150/jca.31703
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发表时间：
2019-01-01
影响因子：
3.9
通讯作者：
Zhou, Guangming
中科院分区：
文献类型：
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作者：
Mao, Weidong;Guo, Ziyang;Zhou, Guangming
长非编码RNA(LncRNAs)通常与肿瘤的发生和发展有关，其中一些在多种人类癌症中表达失调。它们失衡背后的机制值得进一步研究。在这里，我们证明了LNC CRYBG3的表达水平与A549细胞(非小细胞肺癌(NSCLC)细胞)中1501异常表达的蛋白相关。LNC CRYBG3过表达导致M期停滞并促进细胞死亡，而LNC CRYBG3过表达未引起相反的作用。在体外和体内，LNC CRYBG3过表达均可抑制细胞增殖。此外，它还上调细胞周期蛋白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，这些发现提示LNC CRYBG3调控A549细胞的细胞周期过程，提示其在治疗A549疾病方面的潜在应用。
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 in vitro 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.