LINC00261 suppresses human colon cancer progression via sponging miR-324-3p and inactivating the Wnt/β-catenin pathway.

Growing evidence indicates long noncoding RNAs (lncRNAs) are significant regulators in the progression of various malignant tumors including colon cancer. Dysregulation of lncRNA LINC00261 has been identified in many cancers. Investigations on LINC00261 function have revealed that LINC00261 could act as a crucial tumor suppressor in various cancers. But, the biological involvement of LINC00261 in colon cancer is still barely known. Here, we found LINC00261 was reduced in colon cancer cells. Meanwhile, overexpressed LINC00261 repressed colon cancer cell viability and proliferation capacity. In addition, colony cancer cell colony formation was inhibited and apoptosis was enhanced by upregulation of LINC00261. Also, colon cancer cell migration and invasion both were restrained by LINC00261. miR-324-3p can exert important functions in several carcinomas, but its role in colon cancer is uninvestigated. In the current study, miR-324-3p was examined and miR-324-3p was greatly increased in colon cancer cells. Moreover, the association between miR-324-3p and LINC00261 was confirmed via performing RNA immunoprecipitation and RNA-pull-down experiments. In cancer biology, aberrant modulation of the Wnt signaling pathway remains a prevalent theme. Overexpression of LINC00261 obviously impaired colon cancer progression via inactivating the Wnt pathway. Furthermore, in the xenograft model assay, an increase of LINC00261 could suppress colon tumor growth via sponging miR-324-3p and inactivating the Wnt pathway. Overall, our results showed that LINC00261 repressed colon cancer progression via regulating miR-324-3p and the Wnt pathway. LINC00261 could be established as a novel therapeutic target for colon cancer.