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miR‐454 performs tumor‐promoting effects in oral squamous cell carcinoma via reducing NR3C2
Author(s) -
Guo JingYu,
Wang YuKun,
Lv Bo,
Jin Hong
Publication year - 2020
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.13015
Subject(s) - biology , downregulation and upregulation , gene silencing , cell culture , cell growth , cancer research , microrna , transfection , cell , basal cell , subfamily , medicine , genetics , gene
Background Aberrant miRNAs expression regulates the occurrence and progression of a variety of cancers, including oral squamous cell carcinoma (OSCC). This study aims to illustrate the potential effects of miR‐454/nuclear receptor subfamily 3 group C member 2 (NR3C2) on the biological behaviors of OSCC cells. Methods GEO database was applied to detect and analyze the expression of miR‐545 and NR3C2 in OSCC tissues. Two OSCC cell lines including CAL27 and Tca‐83 were utilized to determine the function of miR‐454/NR3C2 on OSCC cells biological behaviors. miR‐454 and NR3C2 expressions were regulated by miR‐454 mimic/inhibitor and pcDNA3.1‐NR3C2/si‐NR3C2, respectively. Cells biological behaviors were evaluated by cell proliferation, colony formation, and transwell assays. Results The data collected from GEO database indicated that miR‐454 expression was upregulated in OSCC tissues; however, the expression of NR3C2 assumed a downward trend. In vitro experiments, the expression trend of miR‐454 in OSCC cell lines was consistent with that of the trend in tissues, and the OSCC cells growth and movement abilities significantly decreased after miR‐454 depletion. Through co‐transfection experiments, we explored that the abilities of OSCC cell proliferation, colony formation, invasion, and migration obviously reduced after miR‐454 depletion, but these phenomena were mitigated to some extent after NR3C2 silencing. Conclusion The study illustrates that miR‐454 acts as an active regulator to facilitate OSCC cells growth, colony formation, invasion, and migration by targeting NR3C2, which may afford a novel perspective and possibility for the targeted treatment of OSCC.