Dai Juanjuan, Zhou Ning, Wu Rui, Du Jing, Miao Shuang, Gong Kaikai, Yang Lijuan, Chen Weiwei, Li Xuelin, Li Chen, Wu Yan
Cancer Research Institute, Binzhou Medical University Hospital, Binzhou, China.
Department of Otolaryngology Head and Neck Surgery, Binzhou Medical University Hospital, Binzhou, China.
Pathol Oncol Res. 2021 Mar 29;27:610159. doi: 10.3389/pore.2021.610159. eCollection 2021.
Long noncoding RNAs (lncRNAs) play a critical role in the development of lung carcinoma. The mechanism of MALAT1 in lung carcinoma development is not understood very well. This study aimed to investigate the role of MALAT1 in lung carcinoma progression and the mechanism underlying the role of miR-491-5p in the MALAT1 mediated regulation of UBE2C expression. The results indicated that the expression of MALAT1 was often augmented in lung carcinoma cells. Suppression of MALAT1 blocked the proliferation, invasion and migration ability of cancer cells and inhibited the expression of UBE2C. UBE2C restoration attenuated the MALAT1 knockdown-induced anti-cancer effects. Moreover, UBE2C and MALAT1 were indicated as targets of miR-491-5p and inhibition of miR-491-5p restored the MALAT1 knockdown-induced inhibition of the progression of lung carcinoma. Furthermore, MALAT1 sponged miR-491-5p to upregulate UBE2C expression, causing it to act as a competing endogenous RNA. Collectively, MALAT1 downregulation suppressed lung carcinoma progression by regulating the miR-491-5p/UBE2C axis. These results indicate that MALAT1 could be a molecular target for lung carcinoma treatment and prognosis.
长链非编码RNA(lncRNAs)在肺癌发展过程中发挥着关键作用。MALAT1在肺癌发展中的机制尚未完全明确。本研究旨在探讨MALAT1在肺癌进展中的作用以及miR-491-5p在MALAT1介导的UBE2C表达调控中作用的潜在机制。结果表明,MALAT1的表达在肺癌细胞中常常升高。抑制MALAT1可阻断癌细胞的增殖、侵袭和迁移能力,并抑制UBE2C的表达。恢复UBE2C的表达可减弱MALAT1敲低诱导的抗癌作用。此外,UBE2C和MALAT1被表明是miR-491-5p的靶点,抑制miR-491-5p可恢复MALAT1敲低诱导的肺癌进展抑制作用。此外,MALAT1可吸附miR-491-5p以上调UBE2C的表达,使其作为竞争性内源RNA发挥作用。总体而言,MALAT1的下调通过调节miR-491-5p/UBE2C轴抑制肺癌进展。这些结果表明,MALAT1可能是肺癌治疗和预后的一个分子靶点。