LINC00665 activates Wnt/β-catenin signaling pathway to facilitate tumor progression of colorectal cancer via upregulating CTNNB1

Background LINC00665 is a newly identified oncogene, which has been reported to be oncogene in various cancers. Nevertheless, its role in the progression of colorectal cancer (CRC) remains obscure to the extent. This study aimed at exploring the role and mechanism of LINC00665 in CRC progression. Materials and methods RNA and protein expression were detected via qRT-PCR and western blot. Functional assays were conducted to investigate the role of LINC00665 in the CRC cellular processes. TOP/FOP assay was performed to detect the activity of Wnt/beta-catenin signaling pathway. Mechanism investigations were carried out to explore the regulatory relationship among genes. Results LINC00665 was overtly expressed in CRC cell lines at high levels. Functionally, silencing of LINC00665 could curb in vitro CRC cell growth, migration and invasion, while stimulating cell apoptosis. Mechanically, LINC00665 sponged miR-214-3p to up-regulate CTNNB1 expression, consequently activating Wnt/beta-catenin signaling pathway. Furthermore, LINC00665 could bind to U2AF2 and enhance the association between U2AF2 and CTNNB1, increasing the stability of CTNNB1. CTNNB1 overexpression could reverse the suppressive effects of LINC00665 downregulation. Conclusion LINC00665 stimulates CRC progression through the activation of Wnt/beta-catenin signaling pathway, which hopefully might be a therapeutic target for CRC.

Automated summary

The study found that LINC00665 is overexpressed in CRC cell lines and can up-regulate CTNNB1 expression by sponging miR-214-3p, thereby activating the Wnt/beta-catenin signaling pathway and promoting CRC cell proliferation, migration and invasion, as well as increasing the stability of CTNNB1. Overexpression of CTNNB1 can reverse the inhibitory effects of LINC00665 downregulation on CRC cells.