Linc00883 affects colorectal cancer through miR-577/FKBP14 axis: a novel mechanism for regulating colorectal cancer cell proliferation, invasion, and migration

Abstract

ABSTRACT Long non-coding RNAs (lncRNAs) are relevant to the development of human cancers. Here, we aimed to investigate the role and mechanism of Linc00883 in the proliferation, invasion, and migration of colorectal cancer (CRC) cells. CRC cell lines SW480 and LoVo were applied as in vitro models in this study. Quantitative real-time PCR was applied to measure Linc00883, miR-577, and FKBP14 expressions. Cell Counting Kit-8, transwell, and wound-healing assays were carried out to confirm the function of Linc00883. Western blot was applied to detect the protein levels of the epithelial–mesenchymal transition-related proteins E-cadherin, vimentin, fibronectin, and α-SMA. RNA immunoprecipitation (RIP) and RNA pull-down experiments were performed to confirm the relationship between Linc00883 and miR-577. Linc00883 expression was elevated in CRC tissues and cells, and the patients with high expression of Linc00883 were related to a low survival rate and prone to distant metastasis. Moreover, we corroborated that Linc00883 and miR-577, miR-577 and FKBP14 are bound to each other. Linc00883 was negatively correlated with miR-577, and miR-577 was also negatively correlated with FKBP14. Furthermore, interference with Linc00883 restrained the proliferation, invasion, and migration of CRC cells through the miR-577/FKBP14 axis. In vivo studies also clarified that Linc00883 facilitated the growth of CRC tumors and the epithelial–mesenchymal transition (EMT) of CRC. Our results demonstrated that Linc00883 facilitated the proliferation, invasion, and migration of CRC cells by regulating the miR-577/FKBP14 axis.