摘要

Background Berberine, a non-prescription medicine clinically applied for diarrhoea and gastroenteritis. Recent studies have demonstrated that it possesses anti-tumour properties in colorectal cancer, but the exact molecular mechanism remains obscure. @@@ Objectives To elucidate the underly molecular mechanisms of berberine in colorectal cancer from a perspective of epigenetics, and tried to explore the role of lincROR-Wnt/beta-catenin molecular axis in the berberine induced the anti-tumour activity in colorectal cancer. @@@ Methods The effects of berberine on cell growth, cell cycle and apoptosis were examined in CRC cells. The in vivo effect of berberine on tumour growth was investigated using a xenograft mice model. Moreover, lincROR and Wnt/beta-catenin signalling were detected by luciferase activity, qRT-PCR and western blotting assays. @@@ Key findings Berberine suppressed cell growth in vitro via inducing cell cycle arrest and apoptosis in CRC cell, and inhibited tumourigenesis in vivo. LincROR was significantly down-regulated by berberine, inducing the inactivation of the canonical Wnt/beta-catenin signalling, meanwhile, the overexpression of lincROR partially reversed the suppressive effects on tumour growth and Wnt/beta-catenin signalling induced by berberine. @@@ Conclusions Berberine inhibits tumour growth partially via regulating the lincROR-Wnt/beta-catenin regulatory axis, which provides a strategy for the design of anti-tumour drugs for CRC patients after our advanced validation.

  • 单位
    广州中医药大学; 南方医科大学