Solmaz Morovati - Department of Pathobiology, School of Veterinary Medicine, ShirazUniversity, Shiraz, Iran
Ali Mohammadi - Department of Pathobiology, School of Veterinary Medicine, ShirazUniversity, Shiraz, Iran
Amir Ali Heidari - Department of Clinical Sciences, School of Veterinary Medicine,Shiraz University, Shiraz, Iran
Mehdi Asad Sangabi - Department of Pathobiology, School of Veterinary Medicine, ShirazUniversity, Shiraz, Iran

Background: Due to the increasing prevalence of colorectalcancer (CRC) worldwide, new treatment methods can have a significant effect on controlling this disease. Therefore, inthis study, the anticancer effects of the matrix (M) gene of themumps virus, Hoshino strain, were investigated in SW۴۸۰ CRCcancer cells.Methods and results: First, amino acid sequence analysis wasperformed on the M protein to identify any similarities withBcl-۲ family members. Next, SW۴۸۰ cells were individuallyinfected with pcDNA۳ plasmids containing the mumps virusM gene, and the percentage of cell death, activity of caspase ۳and caspase ۷, and expression levels of genes involved in apoptoticpathways (p۵۳, Bax, Bcl-۲, Caspase ۸, and Caspase ۹)were investigated. Sequence alignment suggested that the Bcl-۲ domains may be common between the M protein and Bcl-۲family members, triggering apoptosis in CRC cells. The resultsobtained from the diagnostic methods showed that treatmentwith mumps M protein had higher anticancer effects than thecontrol and pcDNA۳. The percentage of apoptosis in thesegroups showed a significant increase after ۹۶ h compared tothat in the control and pcDNA۳. In addition, the groups treatedwith mumps M protein showed an increase in the activity ofcaspases ۳ and ۷, and in the expression of the Bax/Bcl-۲, Caspase۸, Caspase ۹, and p۵۳ genes compared to the control.Conclusion: s This study showed for the first time that themumps virus M protein could be considered a targeted treatmentfor CRC cancer by inducing apoptotic pathways.

Colorectal cancer; Oncolytic viruses; Matrix;Mumps; pcDNA۳ plasmid