JNK Signaling Pathways and Oncoviruses

Abstract

Oncoviruses utilize the host cell signaling pathways. The role of the host cellular kinases as the main signaling factors in the viral replication and assembly has been reported before. The c-Jun NH2-terminal kinases (JNKs) as members of the mitogen-activated protein kinase (MAPK) family are stress-activated protein kinases that can be triggered by radiation, growth factors, cell stress, and inflammatory cytokines. They are involved in the cell proliferation, migration/invasion, various forms of cell deaths including apoptosis, autophagy, and necroptosis, and also cell survival-mediated cancer therapeutic resistance. The JNK pathway plays a key role in oncoviruses replication process. It can be triggered through viral infection and is involved in the replication of some viruses including herpes viruses and rotaviruses. It plays a key role in oncogenesis mechanism of oncoviruses by influencing both oncogenic events and tumor suppressive mechanisms. The present study aimed to highlight and increase our understanding regarding the effects of JNK pathway on the oncogenesis mechanism of oncoviruses including HBV, HCV, HTLV, HPV, KSHV, and EBV.