Figure 1.

Interplay between oncoviral proteins and the cell cycle regulation leading to PGCC formation. Polyploidy has been described in the context of oncogenic viruses. Indeed, oncoviral proteins were shown to employ multiple cellular mechanisms to induce polyploidy. Those include centrosome overduplication and aberrant mitotic spindle pole formation, as well as abortive mitosis and cell cycle disruptions, The latter being dependent partly on p53 depletion or functional abolition, Rb inactivation or even through p53-independent mechanisms. Not limited to checkpoints abrogation, dysregulation of cell-cycle regulators activities such as polo-like kinase 1 (Plk1) also favor polyploidy induction, in addition to endoreplication and re-replication. Anaphase-promoting complex (APC), budding uninhibited by benzimidazoles 1 (Bub1), cell-division cycle protein 20 (cdc20), cyclin dependent kinase 1 (Cdk1), EBV nuclear antigen (EBNA), large HBV surface protein (LHBs), latency-associated nuclear antigen (LANA), latent membrane protein 1 (LMP1), mitotic arrest deficient 2 (Mad 2), NIMA-related protein kinase 2 (Nek2).