MiR-133b inhibits colorectal cancer metastasis via lncRNA-LUCAT1.

Abstract

Aim: Colorectal cancer (CRC) is a common malignant tumor of the digestive system. Metastasis is the leading cause of poor prognosis of CRC patients, warranting further study of the molecular mechanism of metastasis in CRCand identification of new therapeutic targets. MiR-133b has been proven to play an important role in tumorigenesis by directly targeting coding genes. However, whether miR-133b can regulate tumorigenesis via long noncoding RNA (lncRNA) remains unclear. Methods: We systematically analyzed the expression level and correlation of miR-133b and LUCAT1 in cancer tissues and adjacent tissues from 30 patients with CRC. The effects of miR-133b and LUCAT1 on the invasive ability of CRC cells were detected by a transwell assay. The relationship between miR-133b and LUCAT1 was investigated by cells transfection experiments, rescue experiments and luciferase reporter assays. The binding of LUCAT1 and EZH2 was detected by RNA immunoprecipitation assay. Results: MiR-133b was expressed at low levels in CRC tissues, and LUCAT1 was highly expressed, with an inverse correlation between them. LUCAT1 promoted the migration and invasion of HCT116 and SW620 cells. Overexpression of LUCAT1 attenuated the inhibition of cell migration and invasion induced by miR-133b. However, the dual luciferase assay showed that miR-133b did not directly target LUCAT1. Conclusion: MiR-133b affects CRC metastasis via the LUCAT1/EZH2 complex. MiR-133b and LUCAT1 may be potential targets for antimetastasis therapy in CRC.