Video Experimental Relacionado

Updated: Jan 23, 2026

Orthotopic Transplantation of Syngeneic Lung Adenocarcinoma Cells to Study PD-L1 Expression

Orthotopic Transplantation of Syngeneic Lung Adenocarcinoma Cells to Study PD-L1 Expression

Published on: January 19, 2019

Metilación aberrante limita la inflamación antitumoral en el adenocarcinoma de pulmón al restringir la expresión de

Deepti Agrawal¹, Katarina Cisarova², Sebastian Vosberg^2,3,4,5

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

Science advances

|January 21, 2026

Abstract:

Evasion of programmed cell death is a critical hallmark of cancer. However, the contribution of inflammatory forms of cell death in lung carcinogenesis and their effects on the composition of the tumor-immune microenvironment remain unclear. Our multi-omics analyses of samples from patients with primary lung adenocarcinoma revealed that necrosome signaling is repressed because of reduced expression of receptor-interacting protein kinase 3 (RIPK3). Distinct methylation signatures, both in the RIPK3 promoter and nonpromoter regions, correlated with lower transcription levels of RIPK3. This resulted in limited expression of inflammatory genes, advanced histologic features, reduced immune cell invasion, and decreased patient survival. Mechanistically, we confirmed the tumor-suppressive role of necrosome signaling through the genetic deletion of Ripk3 in two independent, clinically relevant mouse models of lung adenocarcinoma. Functionally, RIPK3 shaped a diverse immune environment by promoting the invasion of innate and adaptive immune cells in patient samples and experimental mice. Thus, RIPK3-mediated inflammatory signaling enhances a diverse immune microenvironment and hinders progression in lung adenocarcinoma.

Palabras clave:

metilación adenocarcinoma de pulmón RIPK3 inflamación microambiente tumoral inmunidad muerte celular supervivencia del paciente señalización necrosoma

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