Canine parvovirus induces G1/S cell cycle arrest that involves EGFR Tyr1086 phosphorylation.

ABSTRACT: Canine parvovirus (CPV) has been used in cancer control as a drug delivery vehicle or anti-tumor reagent due to its multiple natural advantages. However, potential host cell cycle arrest induced by virus infection may impose a big challenge to CPV associated cancer control as it could prevent host cancer cells from undergoing cell lysis and foster them regain viability once the virotherapy was ceased. To explore CPV-induced cell cycle arrest and the underlying mechanism toward improved virotherapeutic design, we focus on epidermal growth factor receptor (EGFR), a cellular receptor interacting with TfR that mediates CPV-host interactions, and alterations on its tyrosine phosphorylation sites in response to CPV infection. We found that CPV could trigger host G1/S cell cycle arrest via the EG

SUBMITTER: Dai X 

PROVIDER: S-EPMC7549965 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature