Hanie Motahary Rad, Zahra Niki Boroujeni and Ahmad Aleyasin
Lung cancer is one the most cause of cancer related deaths in the world. Newcastle Disease Virus (NDV) is an oncolytic and targeted self-amplifying agent that is able to replicates and kills only cancer cells. The strongest limitation of NDV in cancer treatments is due to its angiogenesis effect for tumors formation. The NDV mechanism for angiogenesis has not been described. This study was to evaluate for the first time the anti-angiogenesis effect of DSCR1 lonely and in conjunction with NDV in lung cancer cells. Ectopic expression of DSCR1 was induced by lentiviral transfection to A549 cell line. Transfected A549 was treated with the effective dose of NDV. Total RNA was extracted and cDNA was synthesized to detect DSCR1, VEGF, PCNA, Bax, and Bcl2 genes expressions compare to HPRT expression as a housekeeping gene using SYBR green Real-time PCR assay. Over expression of VEGF was detected in RNA level for the first time in NDV treated cells. Significant fold changes of PCNA, Bax, and Bcl2 showed that NDV used mitochondrial pathway for induction of cell death. In LVDSCR1+ treated cancer cells, DSCR1 ectopic expression acts as an anti-angiogenesis factor, by reducing VEGF and inhibiting angiogenesis signaling pathway. Furthermore, the apoptotic effect for DSCR1 gene was shown for the first time in this study in lung cancer cells. A non-significant change in Bax and Bcl2 gene expression has suggested a lack of intracellular apoptosis pathway activity following DSCR1 over expression in cancer cells. In LVDSCR+ + NDV treated cancer cells, over expression of DSCR1 could modulate angiogenesis effect of NDV by VEGF reduction and accelerate apoptosis induction in cancer cells as well. This finding for the first time suggests the benefit and potential usefulness in simultaneous application of oncolytic viruses and gene therapy in cancer treatment.
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