Enhanced expression of long non-coding RNA Sox2ot promoted cell proliferation and motility in colorectal cancer.

BACKGROUND: Colorectal cancer (CRC) is one of the most common carcinomas throughout the world. Although the diagnostic and therapeutic strategies have made some progression in the treatment of CRC patients, the mortality of CRC remains relatively high. Hence, it is an urgency to find out the detailed mechanisms of how CRC occurs.
METHODS: LncRNA Sox2ot expression was explored in CRC tissues and cell lines by using quantitative real-time PCR (qRT-PCR). Cell proliferation, migration and invasion ability was measured following downregulated expression of lncRNA Sox2ot by siRNA in CRC cells. Furthermore, western blot was used to detected the expression of Cyclin B1, Cdc 25C, N-cadherin, and E-cadherin in si-Sox2ot transfected CRC cells.
RESULTS: We found that lncRNA Sox2ot was increased in CRC tissues and cell lines. High expression of Sox2ot was associated with the progression of CRC patients. Decreased Sox2ot expression inhibited the proliferation capacity and caused cell cycle arrested in G0/G1 phase in CRC cells. The key cell cycle regulators Cyclin B1 and Cdc 25C were consistently downregulated by knockdown of Sox2ot. Furthermore, knockdown of Sox2ot suppressed cell migration and invasion and decreased the expression of mesenchymal protein N-cadherin, while it increased the expression of epithelial protein E-cadherin in CRC cells.
CONCLUSIONS: LncRNA Sox2ot could promoted CRC cell proliferation and motility and associated with the outcome of CRC patients, suggesting Sox2ot could serve as a potential therapeutic target in the treatment of CRC.