Chao Liang1, Jun Wang1, Aihua Liu1, Yunqiang Wu1. 1. Department of General Surgery, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China.
Abstract
BACKGROUND: The importance of long non-coding RNAs (lncRNAs) in the regulation of tumorigenesis has been gradually recognized. The roles of lncRNA cancer susceptibility candidate 15 (CASC15) in cancers have been validated by several independent groups; however, its role in colorectal cancer (CRC) remains to be explored. METHODS: Levels of CASC15 in CRC cells and normal cells were measured using a quantitative real-time polymerase chain reaction method. In vitro functional assays were performed to detect the effects of CASC15 on cell proliferation, invasion and apoptosis. Bioinformatic analyses and luciferase activity assays were conducted to investigate the targets for CASC15. Animal experiments were conducted to analyze the effect of CASC15 on tumor growth in vivo. RESULTS: The CASC15 level is revealed to be significantly elevated in CRC cells compared to that in normal cells. In vitro assays revealed that CASC15 overexpression stimulates cell growth and invasion, whereas its down-expression has opposite effects. Furthermore, CASC15 can bind with microRNA-582-5p (miR-582-5p) to modulate high mobility group box 2 (HMGB2) expression. We also showed that silencing of CASC15 inhibits tumor growth. CONCLUSIONS: In summary, CASC15 overexpression could promote CRC carcinogenesis, indicating that knockdown of CASC15 might be a possible therapeutic measure to hinder carcinogenesis. The results of the present study could help us to understand the mechanisms behind CRC progression.
BACKGROUND: The importance of long non-coding RNAs (lncRNAs) in the regulation of tumorigenesis has been gradually recognized. The roles of lncRNA cancer susceptibility candidate 15 (CASC15) in cancers have been validated by several independent groups; however, its role in colorectal cancer (CRC) remains to be explored. METHODS: Levels of CASC15 in CRC cells and normal cells were measured using a quantitative real-time polymerase chain reaction method. In vitro functional assays were performed to detect the effects of CASC15 on cell proliferation, invasion and apoptosis. Bioinformatic analyses and luciferase activity assays were conducted to investigate the targets for CASC15. Animal experiments were conducted to analyze the effect of CASC15 on tumor growth in vivo. RESULTS: The CASC15 level is revealed to be significantly elevated in CRC cells compared to that in normal cells. In vitro assays revealed that CASC15 overexpression stimulates cell growth and invasion, whereas its down-expression has opposite effects. Furthermore, CASC15 can bind with microRNA-582-5p (miR-582-5p) to modulate high mobility group box 2 (HMGB2) expression. We also showed that silencing of CASC15 inhibits tumor growth. CONCLUSIONS: In summary, CASC15 overexpression could promote CRC carcinogenesis, indicating that knockdown of CASC15 might be a possible therapeutic measure to hinder carcinogenesis. The results of the present study could help us to understand the mechanisms behind CRC progression.