adjunct autophagy suppression may be a promising way to eliminate the resistance of cancer cells to treatment

Background and aim: autophagy is a highly conserved mechanism in eukaryotic cells which removes the dysfunctional organelles from the cell. autophagy has immense physiological and pathological roles in cells. there are a variety of reports showing the dual function of autophagy as a tumor suppression and promotion phenomenon. therefore, targeted therapy approaches like virotherapy can be a promising cancer treatment. vesicular stomatitis virus (vsv) is a well-known oncolytic virus which mutations in its matrix (m) protein including m51r, make it a better candidate for oncotargeting. moreover, beclin-1 is one of the key regulators of autophagy and also apoptosis. methods: in the present study, the level of autophagy markers such as beclin-1 and lc3 were investigated concerning the apoptosis process induction by vsv m-protein. two colorectal cancer cell lines hct116 and sw480 and one normal colon epithelial cell line (fhc) which expressing vsv m51r mutant m-protein were compared regarding autophagy versus apoptosis. all experiments were conducted at least in triplicate. results: the results showed that the elevated level of caspase 3 and reduced amount of beclin-1 in transfected sw480 cells may be an acceptable description for apoptosis. conclusion: in hct116 cells domination of autophagy, plays a supportive mechanism for the cells to survive in response to m51r m-protein stress. suppression of autophagy as an adjunct can be a promising way to eliminate resistance to cancer treatment. we have quantitively evaluated the beclin-1 and lc3-ii as autophagy markers, future evaluation of these two along with other markers like p62 will reduce the limitations of this study.