Consumption of high‐fat diet enhanced the malignant progression of human colon cancer in xenograft mouse model

Abstract

Obesity and diet‐induced overweight have been demonstrated as risk factors of colon cancer. Several studies suggested that loss of E‐cadherin adherent molecule has been associated with epithelial– mesenchymal transition (EMT) and the malignant progression of human colon cancer cells. However, the effects of high fat (HF) diet intake on the expression of E‐cadherin and in vivo malignant progression of human colon cancer have not been demonstrated well yet. Our results indicated that consumption of HF diet (45% of total energy intake) for 4 weeks would induce the tumor growth in human colon cancer HT‐29 cell bearing mice. Bioluminescence imaging analysis also confirmed that consumption of HF diet would stimulate the proliferation of human colon cancer. HF diet modulated the expression of E‐cadherin and β‐catenin in xenograft mouse model. Furthermore, consumption of HF diet enhanced the cellular proliferation through the modulation of proliferating cellular nuclear antigen (PCNA) and p21cip proteins. The possible molecular mechanisms of actions were, in part, through the activation of the MAPK/ERK signaling pathway and the suppression of E‐cadherin adhesion molecule. Take together; these results suggested that consumption of HF diet could modulate the growth and the malignant progression of human colon cancer cells in vivo.