4.4 Article

LncRNA MALAT1 Regulating Lung Carcinoma Progression via the miR-491-5p/UBE2C Axis

期刊

PATHOLOGY & ONCOLOGY RESEARCH
卷 27, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/pore.2021.610159

关键词

MALAT1; miR-491-5p; UBE2C; lung carcinoma; proliferatiom

资金

  1. National Natural Science Foundation of China [81903102, 81601189, 31900441]
  2. Key Research and Development Plan of Shandong Province [2019GSF107099, 2019GSF108174]
  3. Shandong Provincial Pharmaceutical Technology Development Plan [2017WS154, 2017WS155]
  4. Natural Science Foundation of Shandong Province [ZR2018QH004, ZR2017PH028, ZR2018BB024]
  5. Research Foundation of Binzhou Medical University [BY2019KJ04, BY2015KJ10]

向作者/读者索取更多资源

This study found that MALAT1 is upregulated in lung carcinoma cells, and its suppression can block cancer cell proliferation, invasion, and migration, as well as inhibit UBE2C expression. Additionally, MALAT1 regulates UBE2C expression by sponging miR-491-5p, affecting the progression of lung carcinoma.
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.

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