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LncRNA NBAT1 suppresses cell proliferation and migration via miR‐346/GSK‐3β axis in renal carcinoma
Author(s) -
Xue Sheng,
Wang Sheng,
Li Jian,
Guan Han,
Jiang Shengqun,
Guo Yuanyuan,
Li Qingwen
Publication year - 2019
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.2111
Subject(s) - wnt signaling pathway , gene knockdown , competing endogenous rna , cell growth , gsk 3 , viability assay , cell migration , microbiology and biotechnology , cancer research , blot , microrna , chemistry , catenin , cell culture , cell , biology , signal transduction , rna , long non coding rna , gene , biochemistry , genetics
Long non‐coding RNA (LncRNA) neuroblastoma associated transcript 1 (NBAT1) was demonstrated to be significantly downregulated in renal carcinoma (RCC) cells. However, the function and mechanism of NBAT1 in RCC is poorly understood. The expression of NBAT1 and glycogen synthase kinase‐3β (GSK‐3β)‐mediated Wnt/β‐catenin‐related proteins were measured by quantitative real‐time PCR (qRT‐PCR) and western blotting in RCC cell lines. Cell viability, migration, and invasion were estimated by CCK‐8 and Transwell assay. The association of miR‐346 with GSK‐3β expression was verified using luciferase assay. NBAT1 was significantly downregulated in RCC cells, and inhibited RCC cell proliferation, migration, and invasion. Furthermore, NBAT1 negatively regulated miR‐346 expression. In addition, miR‐346 overexpression and the knockdown of GSK‐3β, a direct target of miR‐346 could overturn the inhibitory effect of NBAT1 on Wnt/β‐catenin signaling and cell proliferation, migration, and invasion. NBAT1 functioned as an endogenous sponge by competing for miR‐346 binding to GSK‐3β and therefore alleviated RCC cells.