Open AccessLong noncoding RNA TUG1 promotes renal cell carcinoma cell proliferation, migration and invasion by downregulating microRNA‑196a
Author(s) -
Yang Yang,
Deming Sun,
Jin Yu,
Man Zhang,
Yi C,
Rui Yang,
Bernard Dan,
Aijun Li
Publication year - 2018
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.2018.9608
Subject(s) - oncogene , microrna , biology , mtt assay , cell growth , cancer research , carcinogenesis , long non coding rna , kinase , cell cycle , protein kinase a , microbiology and biotechnology , cell , rna , gene , biochemistry
Long noncoding RNA taurine upregulated gene 1 (lncRNA TUG1) and microRNA‑196a (miR‑196a) have been reported to serve important roles in the development of renal cell carcinoma (RCC). However, their potential mechanisms have not been completely elucidated. The aim of the present study was to clarify the biological functions of lncRNA‑TUG1 and miR‑196a, in addition to investigating the interaction between lncRNA‑TUG1 and microRNA‑196a, providing a novel insight into RCC tumorigenesis. The present study comprised two parts. In the first part, lncRNA‑TUG1 was confirmed as an oncogene, via reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) analysis, MTT assay, flow cytometry analysis, and migration and invasion assays. In the second part, the association between lncRNA‑TUG1 and miR‑196a, and the molecular mechanism, was illustrated via RT‑qPCR analysis, MTT assay, dual luciferase reporter assay and western blotting. The results of the present study demonstrated that lncRNA‑TUG1 was able to promote RCC cell proliferation, migration and invasion in vitro by suppressing miR‑196a. Additionally, lncRNA‑TUG1 achieved its biological functions by regulating the expression levels of RAC‑α serine/threonine‑protein kinase, mitogen‑activated protein kinase and extracellular signal‑regulated kinase via inhibition of miR‑196a. In conclusion, the present findings proposed a novel potential therapeutic target, the lncRNA‑TUG1‑miR‑196a axis, which may be applicable to the treatment of RCC.