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Biological function and mechanism of MALAT-1 in renal cell carcinoma proliferation and apoptosis: role of the MALAT-1–Livin protein interaction

Shaoan Chen,P. Ma,Ying‐Jun Zhao,Bin Li,Shaobo Jiang,H. Xiong,Z. Wang,Hanbo Wang,Xunbo Jin,Chuan Liu

Published 2017 in Journal of Physiological Sciences

ABSTRACT

Long noncoding RNAs (lncRNAs) have been shown to play a critical role in cancer development and progression. LncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) is a kidney cancer-associated onco-lncRNA involved in the progression of renal cell carcinoma (RCC). However, the pathological role of lncRNA MALAT-1 in RCC proliferation and metastasis remains poorly understood. This study was designed to investigate the biological role and mechanism of MALAT-1 in RCC proliferation and metastasis. The experiments were performed in human tissues, renal carcinoma cell lines, and nude mice. The expression of lncRNA MALAT-1, Livin mRNA, and the Livin protein was determined by quantitative real-time PCR (qRT-PCR) or a Western blot. The interaction between MALAT-1 and Livin was evaluated by RNA pull-down and RNA binding protein immunoprecipitation (RIP). Cell viability and apoptosis in RCC cell lines were detected using CCK-8 and TUNEL assays. LncRNA MALAT-1 and the Livin protein were highly expressed in RCC tissues, as well as in RCC 786-O and Caki-1 cell lines. MALAT-1 interference contributed to an increase in cell apoptosis and a reduction in the cell viability of 786-O and Caki-1 cells. The increase in apoptosis by si-MALAT-1 was reversed by overexpression of Livin. The RIP results showed that MALAT-1 promoted the expression of the Livin protein in 786-O and Caki-1 cells by enhancing the stability of the protein. Furthermore, the volume of si-MALAT-1-786-O cell xenograft was significantly suppressed. These data indicate that lncRNA MALAT-1-mediated promotion of RCC proliferation and metastasis may be due to the upregulation of the expression of Livin.

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