Interleukin-6 and Interferon-α Signaling via JAK1-STAT Differentially Regulate Oncolytic versus Cytoprotective Antiviral States.

ABSTRACT: Malignancy-induced alterations to cytokine signaling in tumor cells differentially regulate their interactions with the immune system and oncolytic viruses. The abundance of inflammatory cytokines in the tumor microenvironment suggests that such signaling plays key roles in tumor development and therapy efficacy. The JAK-STAT axis transduces signals of interleukin-6 (IL-6) and interferons (IFNs), mediates antiviral responses, and is frequently altered in prostate cancer (PCa) cells. However, how activation of JAK-STAT signaling with different cytokines regulates interactions between oncolytic viruses and PCa cells is not known. Here, we employ LNCaP PCa cells, expressing (or not) JAK1, activated (or not) with IFNs (α or γ) or IL-6, and infected with RNA viruses of different oncolytic poten

SUBMITTER: Danziger O 

PROVIDER: S-EPMC5797546 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature