The duality of STAT2 mediated type I interferon signaling in the tumor microenvironment and chemoresistance

Jorge Canar, Kennedy Darling, Ryan Dadey, Ana M. Gamero

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

Abstract

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.

Original languageEnglish
Article number156081
Pages (from-to)156081
JournalCytokine
Volume161
DOIs
StatePublished - Jan 2023

Keywords

  • Drug Resistance, Neoplasm
  • Ecosystem
  • Interferon Type I/metabolism
  • Janus Kinases/metabolism
  • STAT Transcription Factors/metabolism
  • STAT1 Transcription Factor/metabolism
  • STAT2 Transcription Factor/metabolism
  • Signal Transduction
  • Tumor Microenvironment

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