
Downregulation of long non-coding RNA TRIM52-AS1 functions as a tumor suppressor in renal cell carcinoma
Author(s) -
Zan Liu,
Haiyan Yan,
Shunyao Xia,
Cheng Zhang,
Youcheng Xiu
Publication year - 2016
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2016.4908
Subject(s) - biology , oncogene , cell growth , cancer research , cell cycle , apoptosis , cell , downregulation and upregulation , cell migration , long non coding rna , tumor progression , microbiology and biotechnology , cancer , gene , genetics
Long non-coding RNAs (lncRNAs) are important regulators of gene expression, interacting with the major pathways of cell growth, proliferation, differentiation and survival. Alterations in the function of lncRNAs promote tumor formation, progression and metastasis. The purpose of the present study was to identify novel tumor suppressor lncRNAs, and elucidate their physiological function and mechanism in renal cell carcinoma (RCC). The results of the present study revealed that the expression of the lncRNA, TRIM52‑AS1, was downregulated in RCC, which was demonstrated using reverse transcription‑quantitative polymerase chain reaction analysis. Furthermore, the effects of TRIM52‑AS1 on proliferation, cell migration and apoptosis were analyzed using a wound scratch assay, a 3‑(4,5‑dimethylthiazol‑2yl)‑2,5‑diphenyl tetrazolium bromide assay and flow cytometric analysis, respectively. The overexpression of TRIM52‑AS1 using a synthesized vector significantly suppressed cell migration and proliferation, and induced apoptosis of the RCC cells in vitro, and interference of its expression led to the opposite effects. The present study was the first, to the best of our knowledge, to demonstrate that TRIM52‑AS1 functions as a tumor suppressor in RCC. Further investigation is required to elucidate the molecular mechanisms underlying the effects of TRIM52-AS1 in the development of RCC.