LINC00882 Plays a Tumor-promoter Role in Colorectal Cancer by Targeting miR-3619-5p to Up-regulate CTNNB1

Abstract

Background: Colorectal cancer (CRC) is a common malignant tumor in gastrointestinal tract around the world. Emerging evidence has confirmed that long non-coding RNAs (lncRNAs) are closely connected to cell progression in cancers, including CRC.

Methods: RT-qPCR assays were applied to detect the expression of LINC00882, miR-3619-5p and CTNNB1. Western blot assays were performed to measure the protein level of E-cadherin, N-cadherin and CTNNB1. Transwell assay was conducted to test the cell migration. Immunofluorescence (IF) assay was performed to measure the connected protein of EMT process.

Results: LINC00882 was highly expressed in CRC tissues and cell lines. Knockdown of LINC00882 hindered the process of CRC. Studies on gain-of-function and loss-of-function further testified that knockdown of LINC00882 or up-regulation of miR-3619-5p hindered cell migration and EMT process in CRC cells. Moreover, rescue assay proved that the inhibition of migration ability and EMT process resulted from LINC00882 silencing could be rescued when miR-3619-5p inhibitor or pcDNA3.1/CTNNB1 was transfected into CRC cells.

Conclusion: Our data suggested that LINC00882 promoted the progression of CRC as a ceRNA to regulate CTNNB1 via sponging miR-3619-5p. This finding would supply a novel insight for CRC therapy.

Keywords: CTNNB1; Colorectal cancer; LINC00882; miR-3619-5p.