Trefoil factor 3 knock-down prevents autophagy-related gene 12 elevation in colon adenocarcinoma

Abstract

Colon cancer, which is considered a common gastrointestinal cancer, has been the third leading cause of cancer mortality in the United States. Colon cancer has various histological sub-types and 90% of them are adenocarcinoma. In recent years, autophagy, the process by which cells are self-cannibalized, has been implicated in pathophysiology of various diseases including colon adenocarcinoma and thus, has become a strong research focus. This has also been true for trefoil factor 3 (TFF3). TFF3 is a small secreted peptide that is present in almost all mucin-secreting tissues, it is most abundant in goblet cells of the gastrointestinal tract and expressed at high protein levels in colon cancer. The present study analyzed the expression of TFF3 and autophagy-related gene ATG12 in cancerous and normal tissue samples collected from patients with colon adenocarcinoma. The expression of both proteins was shown to be increased in cancerous as compared to adjacent non-cancerous tissues. Furthermore, these proteins were shown to be positively correlated using the Pearson's Correlation test in cancerous tissues. Finally, TFF3 was shown to regulate ATG12 in human colon adenocarcinoma cells in vitro. Thus, the data presented here suggest that both TFF3 and ATG12 may be promising potential therapeutic targets to develop novel treatment strategies for patients with colon adenocarcinoma.

Keywords: ATG12; TFF3; Western blot; autophagy; colon adenocarcinoma; immunohistochemistry; siRNA.