Abstract
The pathological roles of long non-coding RNAs (lncRNAs) in colorectal carcinoma (CRC) have been corroborated. To date, the pathological contributions of LINC01315 in the epithelial-mesenchymal transition (EMT) property of CRC are still ambiguous. By silencing LINC01315, we disclosed that LINC01315 promoted the growth, metastatic characteristics, and the EMT of CRC cells in vitro. Mechanistically, LINC01315 activated Wnt/β-catenin signaling. LINC01315 bound to the β-catenin promoter and activated its transcription. In rescue experiments, ectopic overexpression of β-catenin counteracted the inhibiting effector-triggered by LINC01315 deletion. In summary, this preliminary study brings new insights to the pathological significance of the LINC01315/Wnt/β-catenin signaling pathway in CRC.