TY - JOUR
T1 - The duality of STAT2 mediated type I interferon signaling in the tumor microenvironment and chemoresistance
AU - Canar, Jorge
AU - Darling, Kennedy
AU - Dadey, Ryan
AU - Gamero, Ana M.
N1 - Publisher Copyright:
© 2022 The Author(s)
PY - 2023/1
Y1 - 2023/1
N2 - The tumor microenvironment consists of tumor cells, extracellular matrix, blood vessels, and non-tumor cells such as fibroblasts and immune cells. Crosstalk among components of this cellular ecosystem can transform non-malignant cells and promote tumor invasion and metastasis. Evidence is accumulating that the transcription factor STAT2, a downstream effector of type I interferon (IFN-I) signaling, can either inhibit or promote tumorigenesis depending on the unique environment presented by each type of cancer. STAT2 has long been associated with the canonical JAK/STAT pathway involved in various biological processes including reshaping of the tumor microenvironment and in antitumor immunity. This dichotomous tendency of STAT2 to both inhibit and worsen tumor formation makes the protein a curious, and yet relatively ill-defined player in many cancer pathways involving IFN-I. In this review, we discuss the role of STAT2 in contributing to either a tumorigenic or anti-tumorigenic microenvironment as well as chemoresistance.
AB - The tumor microenvironment consists of tumor cells, extracellular matrix, blood vessels, and non-tumor cells such as fibroblasts and immune cells. Crosstalk among components of this cellular ecosystem can transform non-malignant cells and promote tumor invasion and metastasis. Evidence is accumulating that the transcription factor STAT2, a downstream effector of type I interferon (IFN-I) signaling, can either inhibit or promote tumorigenesis depending on the unique environment presented by each type of cancer. STAT2 has long been associated with the canonical JAK/STAT pathway involved in various biological processes including reshaping of the tumor microenvironment and in antitumor immunity. This dichotomous tendency of STAT2 to both inhibit and worsen tumor formation makes the protein a curious, and yet relatively ill-defined player in many cancer pathways involving IFN-I. In this review, we discuss the role of STAT2 in contributing to either a tumorigenic or anti-tumorigenic microenvironment as well as chemoresistance.
KW - Drug Resistance, Neoplasm
KW - Ecosystem
KW - Interferon Type I/metabolism
KW - Janus Kinases/metabolism
KW - STAT Transcription Factors/metabolism
KW - STAT1 Transcription Factor/metabolism
KW - STAT2 Transcription Factor/metabolism
KW - Signal Transduction
KW - Tumor Microenvironment
UR - http://www.scopus.com/inward/record.url?scp=85141001683&partnerID=8YFLogxK
U2 - 10.1016/j.cyto.2022.156081
DO - 10.1016/j.cyto.2022.156081
M3 - Article
C2 - 36327541
AN - SCOPUS:85141001683
SN - 1043-4666
VL - 161
SP - 156081
JO - Cytokine
JF - Cytokine
M1 - 156081
ER -
