Abstract
Long non-coding RNAs (lncRNAs) have recently emerged as key regulators of the occurrence and progression of various human cancers, including colorectal cancer. However, the regulatory mechanism of lncRNAs in the tumorigenesis of colorectal cancer remains poorly understood. In this study, we aimed to elucidate the potential role of lncRNA HCG18 in colorectal cancer. Herein, we found that HCG18 expression was significantly upregulated in colorectal cancer tissues and cell lines. Knockdown of HCG18 significantly inhibited the growth and invasion of colorectal cancer cells, while its overexpression had the opposite effect. Moreover, HCG18 was identified as a sponge of miR-1271. Our results showed that knockdown of HCG18 markedly upregulated miR-1271 expression in colorectal cancer cells. Notably, HCG18 expression was inversely correlated with miR-1271 expression in colorectal cancer specimens. Further investigation revealed that HCG18 contributed to the enhancement of MTDH/Wnt/β-catenin signalling in colorectal cancer cells. The antitumour effect of HCG18 inhibition was significantly reversed by miR-1271 inhibition or MTDH overexpression. Overall, the results of our study demonstrate that HCG18 exerts a potential oncogenic function in colorectal cancer by enhancing MTDH/Wnt/β-catenin signalling via sponging of miR-1271, highlighting the importance of HCG18/miR-1271/ MTDH/Wnt/β-catenin signalling in the progression of colorectal cancer.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: Clinical and Experimental Pharmacology and Physiology
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.