LncRNA CCAT1 inhibits cell apoptosis of renal cell carcinoma through up-regulation of Livin protein

• Published in: Molecular and cellular biochemistry 2017-10, Vol.434 (1-2), p.135-142
• Main Authors: Chen, Shaoan, Ma, Pengpeng, Li, Bin, Zhu, Dawei, Chen, Xiude, Xiang, Yuzhu, Wang, Tengteng, Ren, Xiangbin, Liu, Chuan, Jin, Xunbo
• Format: Article
• Language: English
• Subjects: Analysis; Animal models; Apoptosis; Assaying; Biochemistry; Biomedical and Life Sciences; Bromine compounds; Cancer; Cardiology; Cells; Colon; Colon cancer; DNA nucleotidylexotransferase; DNA polymerases; Immunoprecipitation; In vitro methods and tests; Kidney cancer; Kidneys; Life Sciences; Medical Biochemistry; Non-coding RNA; Nucleotide sequence; Oncology; Protein binding; Proteins; Renal cell carcinoma; Ribonucleic acid; RNA; RNA-binding protein; RNA-mediated interference; Transcription; Up-regulation
• ISSN: 0300-8177; 1573-4919
• DOI: 10.1007/s11010-017-3043-8

This study was to investigate the involvement of long non-coding RNA (lncRNA) colon cancer-associated transcript-1 (CCAT1) in renal cell carcinoma (RCC) and to further uncover its underlying mechanism. In this study, the expression of CCAT1 and Livin of RCC tissues or cells was determined using qRT-PCR (quantitative real-time PCR) and western blot, respectively. RNA pulldown and RIP (RNA-Binding Protein Immunoprecipitation) assays were performed to examine the sequence interaction between CCAT1 and Livin. The viability and apoptosis of RCC cells was assessed by MTT(3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and TUNEL (TdT-mediated dUTP nick end labeling) assays, respectively. Mice of tumor animal models were established to observe the effect of CCAT1 on RCC tumor growth. The relative expression of CCAT1 in RCC tissues and cell lines was obviously higher than that of the control. CCAT1 knockdown could reduce cell viability and increase the apoptosis of RCC cells in vitro. Furthermore, Livin was significantly inhibited by CCAT1 silencing; RNA pulldown and RIP assays showed that CCAT1 was physically associated with Livin protein. Moreover, Livin overexpression not only significantly inhibited RCC cell apoptosis and increased cell viability, but completely reversed the si-CCAT1-mediated repression of cell viability. More importantly, CCAT1 silencing could inhibit the growth of RCC in vivo that was accompanied by the reduction of Livin in RCC tissues. CCAT1 inhibits RCC cell apoptosis and increases cell viability through up-regulation of Livin.