Down regulation of the long non-coding RNA PCAT-1 induced growth arrest and apoptosis of colorectal cancer cells

• DOI: 10.1016/j.lfs.2017.08.024
• Publication Date: 2017-08-30T21:31:13Z
• Authors: Lei Qiao; Xiangyu Liu; Yichao Tang; Zheng Zhao; Jilong Zhang; Yong Feng
• Keywords: Male; 0301 basic medicine; 0303 health sciences; Cell Cycle; Down-Regulation; Apoptosis; Xenograft Model Antitumor Assays; 3. Good health; Proto-Oncogene Proteins c-myc; Mice; 03 medical and health sciences; Cell Line, Tumor; Cyclins; Animals; Humans; RNA, Long Noncoding; RNA, Small Interfering; Apoptosis Regulatory Proteins; Colorectal Neoplasms; Cell Proliferation

The long non-coding RNA (lncRNA) was reported to be involved in the progress of various cancers, however, its effect in colorectal cancer (CRC) remains unknown. The goal of the present study is to investigate the function role of lncRNA PCAT-1 in colorectal cancer.The expression of lncRNA PCAT-1 in four CRC cell lines was measured by real-time PCR, and two lncRNA PCAT-1 high expression cell lines were selected. LncRNA PCAT-1 in these two CRC cell lines was down-regulated by shRNA, and the stable transfected cells were established. Functional involvement of lncRNA PCAT-1 in proliferation and apoptosis of the two CRC cells were evaluated in vitro. Mover, the effect of lncRNA PCAT-1 in tumor proliferation was also evaluated in CRC cell xenograft.The results showed that down-regulation of lncRNA PCAT-1 in CRC cells inhibited proliferation, blocked cell cycle transition, and suppressed the expression of cyclins and c-myc. The apoptosis cell proportion was elevated with increased expression of pro-apoptotic proteins and decreased anti-apoptotic proteins in lncRNA PCAT-1 knock down cells. Forced over-expression of c-myc in PCAT-1 down-regulated CRC cells increased the level of cyclins. The xenograft growth in lncRNA PCAT-1 down-regulated cells was significantly inhibited along with the reduced proliferative cells.Our study revealed a tumorigenic effect of lncRNA PCAT-1 in CRC cells, and this effect is partly dependent on the inhibition of c-myc.