Abstract
Colorectal carcinoma (CRC) continues to be a major problem in developed countries, and successful preventive strategies concerning this malignancy are still missing. Sodium selenite has emerged as a potential chemopreventive agent due to a number of specials effects which produce colon cancer cells, regardless of their status.
Selenite has been able to decrease cell proliferation and induce cytotoxicity by several mechanisms. These include direct inhibition of several molecular targets, signaling pathways (p53-dependent, mTOR, p38, JNK), or subcellular compartments (mitochondria), as well as activation of apoptosis and autophagy.
Our data combined with results of studies conducted by other reserarch groups demonstrate a close connection between selenite-induced oxidative stress and apoptosis. In addition, the concurrent existence of autophagy and apoptosis in selenite-treated cells, their mutual relationship, and diverse regulatory patterns upon differing p53 status of cells suggest a multilevel regulation of both processes which warrants future studies.