Oncolytic effects of S77K matrix protein of Vesicular Stomatitis Virus in Cervical Cancer

Researchers are currently investigating cancer therapies employing anti-tumor viruses, sometimes referred to as oncolytic viruses. These viruses can selectively attack tumor cells while sparing normal cells. The vesicular stomatitis virus (VSV) exhibits anti-tumor capabilities through two apoptotic pathways, contingent upon the specific cell line under investigation. The matrix protein of VSV is capable of apoptosis induction in HeLa cells, independent of other virus components, leading to cell death. This study aimed to compare the apoptosis induced by native VSV matrix proteins with that induced by mutant VSV matrix proteins. The mutant VSV matrix protein was prepared by replacing Ser with Lys at amino acid residue 89 (S89K). Following the cloning of both normal and mutant forms of the matrix gene into the EGFP-pcDNA3.1 (+) expression vector, the constructs were individually transfected into HeLa cells, and their expression was confirmed via fluorescence microscopy. The apoptosis rate was subsequently assessed and compared by means of flow cytometry. The VSV matrix protein could induce apoptosis in cell culture, and the highest induction was witnessed at 48 hours post-transfection. The findings demonstrated that the apoptotic efficacy of the VSV matrix protein increased following the substitution of alcoholic amino acids with basic amino acids in the S89K mutant. The present work induced a particular mutation at a specified site to improve the VSV matrix protein's apoptotic capabilities and found that it increases apoptosis induction. This feature is essential for producing desired mutations in recombinant viruses to create anticancer vaccines targeting particular cell lines.