Journal
ONCOTARGET
Volume 7, Issue 23, Pages 34011-34021Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.8514
Keywords
miR-486-5p; CDK4; NSCLC; methylation; cell cycle
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Funding
- Shanghai Municipal Natural Science Foundation [31170750, 81001037, 2013ZX09103001-009, 10ZR1428100]
- foundation from State Key Laboratory of Cell Biology
- foundation from state key laboratory of molecular biology
- Institute of Biochemistry and cell Biology
- Shanghai Institutes for life Sciences, Chinese Academy of Sciences
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MicroRNAs are a class of non-coding single-stranded RNA, 20-23 nucleotide in length, which can be involved in the regulation of gene expression. Through binding with 3'-untranslated regions (3'-UTR), microRNAs can cause degradation of target mRNAs or inhibition of translation, and thus regulating the expression of genes at the post-transcriptional level. In this study, we found that miR-486-5p was significantly downregulated in non-small cell lung cancer (NSCLC) tissues and cell lines, suggesting that miR-486-5p might function as a tumor suppressor in lung cancer. Additionally, we showed that CDK4, an oncogene that plays an important role in cell cycle G1/S phase progression, was directly targeted by miR-486-5p. Furthermore, our data reveals that knockdown of CDK4 by siRNA can inhibit cell proliferation, promote apoptosis, and impede cell-cycle progression. In epigenetics, the upstream promoter of miR-486-5p was strongly regulated by methylation in NSCLC. Collectively, our results suggest that miR-486-5p could not only inhibit NSCLC by downregulating the expression of CDK4, but also be as a promising and potent therapy in the near future.
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