SOCS3 deregulation contributes to aberrant activation of the JAK/STAT pathway in precursor T-cell neoplasms

Br J Haematol. 2023 May;201(4):718-724. doi: 10.1111/bjh.18694. Epub 2023 Feb 14.

Abstract

Despite the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway being frequently altered in T-ALL/LBL, no specific therapy has been approved for T-ALL/LBL patients with constitutive signalling by JAK/STAT, so there is an urgent need to identify pathway members that may be potential therapeutic targets. In the present study, we searched for JAK/STAT pathway members potentially modulated through aberrant methylation and identified SOCS3 hypermethylation as a recurrent event in T-ALL/LBL. Additionally, we explored the implications of SOCS3 deregulation in T-ALL/LBL and demonstrated that SOCS3 counteracts the constitutive activation of the JAK/STAT pathway through different molecular mechanisms. Therefore, SOCS3 emerges as a potential therapeutic target in T-ALL/LBL.

Keywords: JAK/STAT pathway; SOCS3; precursor T-cell neoplasms (T-ALL/LBL).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Humans
  • Janus Kinases / metabolism
  • Leukemia-Lymphoma, Adult T-Cell*
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma*
  • STAT Transcription Factors / metabolism
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction
  • Suppressor of Cytokine Signaling 3 Protein / genetics
  • Suppressor of Cytokine Signaling 3 Protein / metabolism
  • Suppressor of Cytokine Signaling Proteins / metabolism
  • T-Lymphocytes / metabolism

Substances

  • Janus Kinases
  • Suppressor of Cytokine Signaling 3 Protein
  • STAT Transcription Factors
  • STAT3 Transcription Factor
  • Suppressor of Cytokine Signaling Proteins
  • SOCS3 protein, human