Targeting the JAK2/STAT3 Pathway-Can We Compare It to the Two Faces of the God Janus?

Int J Mol Sci. 2020 Nov 4;21(21):8261. doi: 10.3390/ijms21218261.

Abstract

Muscle cachexia is one of the most critical unmet medical needs. Identifying the molecular background of cancer-induced muscle loss revealed a promising possibility of new therapeutic targets and new drug development. In this review, we will define the signal transducer and activator of transcription 3 (STAT3) protein's role in the tumor formation process and summarize the role of STAT3 in skeletal muscle cachexia. Finally, we will discuss a vast therapeutic potential for the STAT3-inhibiting single-agent treatment innovation that, as the desired outcome, could block tumor growth and generally prevent muscle cachexia.

Keywords: muscle cachexia; pSTAT3 inhibitors; targeted therapy.

Publication types

  • Review

MeSH terms

  • Animals
  • Cachexia / drug therapy*
  • Cachexia / etiology
  • Cachexia / metabolism
  • Humans
  • Janus Kinase 2* / antagonists & inhibitors
  • Janus Kinase 2* / metabolism
  • Janus Kinase 2* / physiology
  • Molecular Targeted Therapy / methods*
  • Molecular Targeted Therapy / trends
  • Muscle, Skeletal / metabolism
  • Muscle, Skeletal / pathology
  • Muscular Atrophy / drug therapy*
  • Muscular Atrophy / etiology
  • Muscular Atrophy / metabolism
  • Neoplasms / complications
  • Neoplasms / drug therapy
  • Neoplasms / metabolism
  • Neoplasms / pathology
  • Phosphorylation / drug effects
  • Protein Kinase Inhibitors / pharmacology
  • STAT3 Transcription Factor* / antagonists & inhibitors
  • STAT3 Transcription Factor* / metabolism
  • STAT3 Transcription Factor* / physiology
  • Signal Transduction / drug effects
  • Signal Transduction / physiology

Substances

  • Protein Kinase Inhibitors
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • JAK2 protein, human
  • Janus Kinase 2