C Xi1, N-Y Ye, Y-B Wang. 1. Department of General Surgery, Wujin Hospital Affiliated with Jiangsu University, the Wujin Clinical College of Xuzhou Medical University, Changzhou, China. yibowang@wjxmu.com.
Abstract
OBJECTIVE: Long non-coding RNAs (lncRNAs) play vital roles in the pathogenesis and development of multiple cancers, including colorectal cancer (CRC). Nevertheless, the regulatory mechanisms of LINC01278 in CRC remain unknown. Our research aims to identify the regulatory mechanisms of LINC01278 in CRC. PATIENTS AND METHODS: The expression of LINC01278 was examined by quantitative real-time polymerase chain reaction (RT-qPCR). StarBase and TargetScan websites were used to predict the interaction between miR-134 and LINC01278 or KDM2A, which was further confirmed by Dual-Luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Cell viability, migration, and invasion were detected by Cell Counting Kit-8 (CCK-8) and transwell assays. RESULTS: LINC01278 was upregulated in CRC tissues and cell lines, and knockdown of LINC01278 suppressed CRC cell progression. In addition, LINC01278 inhibited miR-134 expression by direct interaction, and the inhibition of miR-134 abolished the suppressive effects of LINC01278 knockdown on viability, migration, and invasion of CRC cells. Furthermore, KDM2A was confirmed to be a target gene of miR-134. Overexpression of KDM2A facilitated the tumorigenesis of CRC, while this effect was reversed by the upregulation of miR-143. Finally, it was demonstrated that miR-134 inhibitor reversed the shLINC01278‑mediated inhibitory effect on KDM2A expression. CONCLUSIONS: Our study demonstrated that LINC01278 upregulated KDM2A to promote CRC progression by interacting with miR-143, suggesting that LINC01278 might be a new therapeutic target of CRC.
OBJECTIVE: Long non-coding RNAs (lncRNAs) play vital roles in the pathogenesis and development of multiple cancers, including colorectal cancer (CRC). Nevertheless, the regulatory mechanisms of LINC01278 in CRC remain unknown. Our research aims to identify the regulatory mechanisms of LINC01278 in CRC. PATIENTS AND METHODS: The expression of LINC01278 was examined by quantitative real-time polymerase chain reaction (RT-qPCR). StarBase and TargetScan websites were used to predict the interaction between miR-134 and LINC01278 or KDM2A, which was further confirmed by Dual-Luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Cell viability, migration, and invasion were detected by Cell Counting Kit-8 (CCK-8) and transwell assays. RESULTS:LINC01278 was upregulated in CRC tissues and cell lines, and knockdown of LINC01278 suppressed CRC cell progression. In addition, LINC01278 inhibited miR-134 expression by direct interaction, and the inhibition of miR-134 abolished the suppressive effects of LINC01278 knockdown on viability, migration, and invasion of CRC cells. Furthermore, KDM2A was confirmed to be a target gene of miR-134. Overexpression of KDM2A facilitated the tumorigenesis of CRC, while this effect was reversed by the upregulation of miR-143. Finally, it was demonstrated that miR-134 inhibitor reversed the shLINC01278‑mediated inhibitory effect on KDM2A expression. CONCLUSIONS: Our study demonstrated that LINC01278 upregulated KDM2A to promote CRC progression by interacting with miR-143, suggesting that LINC01278 might be a new therapeutic target of CRC.