Absent expression of miR‑30a promotes the growth of lung cancer cells by targeting MEF2D
Author(s) -
Luan Nian-xu,
Yi Wang,
Xuedong Liu
Publication year - 2018
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2018.8719
Subject(s) - oncogene , microrna , lung cancer , western blot , cancer research , biology , transfection , apoptosis , cancer , downregulation and upregulation , untranslated region , cell growth , three prime untranslated region , cancer cell , microbiology and biotechnology , cell cycle , cell culture , messenger rna , gene , oncology , medicine , genetics
The microRNA (miR)-30 family has been reported to be aberrantly expressed in several types of cancer. However, its contributions to lung cancer remain to be fully elucidated. Myocyte enhancer factor 2D (MEF2D), an oncogene in liver cancer, has been shown to be aberrantly expressed in lung cancer. In the present study, it was found that MEF2D and miR-30a were inversely correlated in lung cancer samples. Using an online database, it was predicted that miR-30a targeted the 3' untranslated region (UTR) of MEF2D mRNA. The activity of luciferase with MEF2D 3'UTR was suppressed by transfecting cells with miR-30a mimics. The results of western blot analysis showed that the miR-30a mimics also suppressed the MEF2D protein. The miR-30a mimics were able to reduce the growth and colonies of lung cancer cells by suppressing MEF2D. The results of FACS and western blot assays showed that the apoptotic rate was reduced by transfection with the miR-30a mimics. Collectively, the aberrant expression of miR-30a in lung cancer promoted the expression of MEF2D protein. miR-30a inhibited the growth and colony formation of the lung cancer cells by promoting apoptosis.
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