High glucose induces epithelial-mesenchymal transition and results in the migration and invasion of colorectal cancer cells.

Abstract

Diabetes mellitus (DM) is associated with an increased risk of colorectal cancer (CRC). Hyperglycemia, a chronic abnormality in diabetes, is an independent predictor of cancer-associated mortality in CRC. However, the underlying biological mechanism of hyperglycemia in CRC cells is largely unknown. In the present study, HCT-116 and HT-29 cell proliferation, apoptosis, migration and invasion were assessed. In addition, the expression of epithelial (E)-cadherin, vimentin and high-mobility group A protein 2 (HMGA2) were assessed using western blotting. The results demonstrated that high glucose (HG; 30 mmol/l) caused CRC cells to lose their epithelial morphology, with a decrease in E-cadherin and an increase in vimentin, suggesting epithelial-mesenchymal transition (EMT). Furthermore, HG significantly enhanced the cell migration and invasion of CRC cells and the expression of HMGA2. Transfection with HMGA2 small interfering RNA reversed the HG-induced changes to CRC cells. In addition, HG promoted CRC cell proliferation and suppressed apoptosis. The results of the present study suggest that hyperglycemia promotes EMT, proliferation, migration and invasion in CRC cells and may provide novel insights into the link between HG and CRC.