Harnessing tumorous flaws for immune supremacy: is miRNA-155 the weak link in breast cancer progression?

J Clin Invest. 2022 Oct 3;132(19):e163010. doi: 10.1172/JCI163010.

Abstract

With the advent of immune checkpoint blockade (ICB) therapy, treatment strategies for late-stage cancers have seen a radical advancement. In this issue of the JCI, Wang et al. characterize the functional role of miR-155 in breast cancer and its potential in harnessing the efficacy of immunotherapy. The study reports that high expression levels of miR-155 in breast cancer cells downregulated suppressor of cytokine signaling 1 (SOCS1), increased the phosphorylated STAT1 (pSTAT1)/pSTAT3 ratio, and thereby stimulated chemoattractants for tumor infiltration of effector T cells. Moreover, miR-155 overexpression set the stage for ICB therapy via increased programmed death ligand 1 (PD-L1) expression on cancer cells and enhanced immunological memory response via the release of miR-155-containing extracellular vesicles. Collectively, these data suggest that miR-155 is a strong candidate as a prognostic biomarker for ICB therapy.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Comment

MeSH terms

  • B7-H1 Antigen / metabolism
  • Biomarkers
  • Breast Neoplasms* / drug therapy
  • Breast Neoplasms* / therapy
  • Chemotactic Factors / therapeutic use
  • Cytokines
  • Female
  • Humans
  • Immune Checkpoint Inhibitors
  • Immunotherapy
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism

Substances

  • B7-H1 Antigen
  • Biomarkers
  • Chemotactic Factors
  • Cytokines
  • Immune Checkpoint Inhibitors
  • MIRN155 microRNA, human
  • MicroRNAs