The V protein in oncolytic Newcastle disease virus promotes HepG2 hepatoma cell proliferation at the single-cell level

BackgroundNewcastle disease virus (NDV) is an oncolytic virus that can inhibit cancer cell proliferation and kill cancer cells. The NDV nonstructural V protein can regulate viral replication; however, whether the V protein contributes to NDV oncolysis is unclear.ResultsThis study revealed that NDV inhibited tumor cell proliferation and that V protein expression promoted the proliferation of HepG2 cells, as determined at the single-cell level. In addition, to identify the regulatory mechanism of the V protein in HepG2 cells, transcriptome sequencing was performed and indicated that the expression/activation of multiple cell proliferation-related genes/signaling pathways were changed in cells overexpressing the V protein. Hence, the MAPK and WNT signaling pathways were selected for verification, and after blocking these two signaling pathways with inhibitors, the V protein promotion of cell proliferation was found to be attenuated.ConclusionsThe results showed that the V protein regulated the proliferation of cancer cells through multiple signaling pathways, providing valuable references for future studies on the mechanism by which the V protein regulates cancer cell proliferation.

Automated summary

This study found that Newcastle disease virus (NDV) can inhibit tumor cell proliferation and kill cancer cells. The nonstructural V protein of NDV can regulate viral replication, but its contribution to NDV oncolysis is unclear. The expression of V protein was found to promote the proliferation of HepG2 cells, and transcriptome sequencing revealed changes in the expression/activation of multiple cell proliferation-related genes/signaling pathways in cells overexpressing the V protein. The MAPK and WNT signaling pathways were selected for verification, and blocking these pathways attenuated the promotion of cell proliferation by the V protein.