Circ‐MALAT1 accelerates cell proliferation and epithelial mesenchymal transformation of colorectal cancer through regulating miR‐506‐3p/KAT6B axis

Abstract

AbstractColorectal cancer (CRC) is a prevalent malignant tumor of the digestive tract. Circular RNAs may play important roles in the progression of CRC. In this study, we investigated the roles and mechanisms of action of circ‐MALAT1 in CRC. Gene expression and protein abundance were determined using qRT‐PCR and western blot, respectively. Cell proliferation and migration were assessed by MTT, clone formation, and wound‐healing assays. The interactions among the long non‐coding RNA metastasis‐associated lung adenocarcinoma transcript 1 (circ‐MALAT1), miR‐506‐3p, and lysine acetyltransferase 6B (KAT6B) were predicted using the StarBase software and confirmed by the luciferase activity assay. Circ‐MALAT1 and KAT6B were upregulated, while miR‐506‐3p was downregulated in CRC cells. We validated that knocking down of circ‐MALAT1 suppressed proliferation, migration, and epithelial–mesenchymal transition (EMT) of CRC cells, and these effects were abolished by miR‐506‐3p downregulation or KAT6B sufficiency. Our study suggests that circ‐MALAT1 could sponge miR‐506‐3p to regulate the expression of KAT6B. Moreover, KAT6B sufficiency could neutralize miR‐506‐3p‐dependent growth arrest, migration, and EMT. Circ‐MALAT1 promotes cell proliferation, migration, and EMT of CRC cells via the miR‐506‐3p/KAT6B axis, thereby acting as a novel potential therapeutic target for the treatment of colorectal cancer.