The Role of Vesicular Stomatitis Virus Matrix Protein in Autophagy in the Breast Cancer.

Abstract

Background:Breast cancer is one of the most difficult malignancies to treat. Therapeutics is used to target and kill the cancer cells. Non-human oncolytic viruses have the ability to cause cell death directly to cancers. The objective here was to investigate the role of Vesicular Stomatitis Virus (VSV) Matrix (M) protein in autophagy in the breast cancer cell line. Methods: Two different VSV wild type and mutant (M51R) M protein constructs were produced. Breast cancer cell line BT-20 was transfected by either wild type or mutant vectors. Transfection efficiency was measured using a fluorescent microscopy. Expression of VSV M protein was investigated at protein level. Cell cytotoxicity was measured using an MTT assay. The autophagy pathway was studied by Beclin-1 immunoassay. Data were statistically analyzed between different transfected groups. Results:It has been shown that the VSV M protein induced higher levels of Beclin-1 than the M51R mutant in the BT-20 cell line. Increased levels of Beclin-1 were also associated with VSV M cell-induced cytotoxicity. Conclusion:It has been shown here that VSV wild type or mutant M proteins can cause autophagy-induced cell death by increasing Beclin-1 expression. This includes the possible role of VSV to be used as an oncolytic virus in breast cancer treatment.