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Aberrant methylation limits antitumoral inflammation in lung adenocarcinoma by restricting RIPK3 expression

Deepti Agrawal1, Katarina Cisarova2, Sebastian Vosberg2,3,4,5

  • 1Medical Department III, School of Medicine, Technical University of Munich, Munich, Germany.

Science Advances
|January 21, 2026
PubMed

Insights

Receptor-interacting protein kinase 3 (RIPK3) represses lung adenocarcinoma progression by activating inflammatory cell death and promoting immune cell invasion. Loss of RIPK3 function correlates with poor patient survival.

Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Evasion of programmed cell death is a key cancer mechanism.
  • The role of inflammatory cell death in lung cancer and its impact on the tumor-immune microenvironment are not fully understood.

Purpose of the Study:

  • To investigate the role of necrosome signaling, specifically receptor-interacting protein kinase 3 (RIPK3), in lung adenocarcinoma development.
  • To determine how RIPK3 influences the tumor-immune microenvironment and patient outcomes.

Main Methods:

  • Multi-omics analyses of patient samples.
  • Analysis of RIPK3 promoter and nonpromoter methylation.
  • Genetic deletion of Ripk3 in mouse models of lung adenocarcinoma.

Main Results:

  • Reduced RIPK3 expression, linked to methylation changes, was observed in lung adenocarcinoma.
  • Lower RIPK3 expression correlated with repressed necrosome signaling, limited inflammatory gene expression, advanced histology, reduced immune cell infiltration, and decreased patient survival.
  • Genetic deletion of Ripk3 in mice confirmed its tumor-suppressive role and demonstrated its function in promoting immune cell invasion.

Conclusions:

  • RIPK3-mediated inflammatory signaling is crucial for a diverse immune microenvironment in lung adenocarcinoma.
  • RIPK3 acts as a tumor suppressor by enhancing immune cell infiltration and hindering tumor progression.

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