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Inhibition of anti-tumor immunity by melanoma cell-derived Activin-A depends on STING

Katarina Pinjusic1, Giovanna Ambrosini2,3, Joao Lourenco4

  • 1Ecole Polytechnique Fédérale de Lausanne (EPFL), SV ISREC, Lausanne, Switzerland.

Frontiers in Immunology
|February 2, 2024
PubMed

Insights

Activin A overexpression in melanoma hinders anti-tumor immunity. Targeting STING activity in melanoma cells may overcome this immune evasion and reduce tumor growth.

Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Activin A, a TGF-β family member, is overexpressed in various cancers, linked to cachexia and poor prognosis.
  • Activin A secreted by melanoma cells impairs CD8+ T cell immunity and immunotherapy response, despite its proinflammatory role elsewhere.

Purpose of the Study:

  • To investigate the mechanisms by which Activin A influences melanoma anti-tumor immunity and tumor microenvironment.
  • To explore the potential of targeting STING activity as a therapeutic strategy against Activin A-driven melanoma.

Main Methods:

  • Analysis of syngeneic grafts of Braf mutant YUMM3.3 mouse melanoma cells.
  • Single-cell RNA sequencing to analyze the tumor microenvironment.
  • Investigated the role of STING (Stimulator of Interferon Genes) pathway activity.

Main Results:

  • Activin A induced immune evasion in melanoma, characterized by a proinflammatory interferon signature across multiple cell types.
  • Tumor growth acceleration associated with Activin A was partly dependent on STING activity within melanoma cells.
  • Proinflammatory signals contribute to immune evasion in the tumor microenvironment.

Conclusions:

  • Activin A promotes melanoma immune evasion and tumor growth through mechanisms involving STING activation.
  • STING represents a promising therapeutic target to counteract tumor-promoting Activin A signaling in melanoma.
Keywords:
STINGactivincancerintercellular communicationinterferonknockdownprofilingscRNA-seq

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