Open Access

ARTICLE

Highly Expressed Antisense Noncoding RNA in the INK4 Locus Promotes Growth and Invasion of Renal Clear Carcinoma Cells via the β-Catenin Pathway

Qingchun Li^*, Yuan Tian^†, Guangrui Hu^†, Yun Liang^†, Wei Bai^†, Hongjun Li^†

* Department of Gastrointestinal Colorectal and Anal Surgery, China–Japan Union Hospital of Jilin University, Changchun, P.R. China
† Center of Physical Examination, China–Japan Union Hospital of Jilin University, Changchun, P.R. China

Oncology Research 2017, 25(8), 1373-1382. https://doi.org/10.3727/096504017X14878509668646

Abstract

Long noncoding RNA (lncRNA) antisense noncoding RNA in the INK4 locus (ANRIL) is involved in several human cancers. However, the role of ANRIL in renal cell carcinoma (RCC) remains unclear. This study aimed to explore whether, and how, ANRIL affects the progression of RCC. First, the expression of ANRIL in clinical tumor tissues and four kinds of RCC cell lines was evaluated. After transfection, cell viability, colony number, apoptosis, migration, and invasion were assessed. The expression of proteins related to apoptosis, epithelial-tomesenchymal transition (EMT), and the β-catenin signaling pathway was then assessed. In addition, the effect of IWR-endo (β-catenin inhibitor) on cell viability, migration, and invasion, as well as β-catenin expression, was also evaluated. The results showed that ANRIL was highly expressed in RCC tissues and RCC cell lines. ANRIL significantly promoted cell proliferation, migration, invasion, and EMT but inhibited cell apoptosis. Additionally, the expression levels of β-catenin, Ki-67, glycogen synthase kinase 3β (GSK-3β), phosphorylated GSK-3β, T-cell transcription factor 4 (TCF-4), and leukemia enhancer factor 1 (LEF-1) were all markedly upregulated by ANRIL. The effect of ARNIL silencing was opposite to that of ANRIL overexpression. The effect of ARNIL on proliferation, migration, and invasion of RCC cells was found to be reversed by IWRendo. In conclusion, ANRIL, which is highly expressed in RCC, acted as a carcinogen in RCC cells through the activation of the β-catenin pathway.

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