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Article

Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance.

Cancer immunology research - 2 Jul 2026

Suzuki Sora, Kandar Bojidar, Ting Catrina, Deraska Peter, Chen Te-An, Giridharan Thejaswini, Khan Anm Nazmul H, Attwood Kristopher, Yu Han, Catalfamo Kayla, Singh Prashant K, Bushey Ryan T, Gottlin Elizabeth B, Campa Michael J, Patz Edward F, Ajona Daniel, Pio Ruben, Segal Brahm H, Yau Edwin H

Abstract excerpt

Loss-of-function STK11 mutations occur in 15% to 20% of lung adenocarcinomas (LUAD) and correlate with immunotherapy failure and worse survival. By integrating analysis of human tumor samples, a human LUAD cell line panel, and Cancer Cell Line Encyclopedia and The Cancer Genome Atlas datasets, we found that C3 production was increased in human STK11-mutant versus STK11-wildtype (WT) LUAD, modulated by LKB1 loss,...

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Share to Adenocarcinoma of Lung
Share to AMP-Activated Protein Kinase Kinases

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Complement C3

Share to Drug Resistance, Neoplasm

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Share to Lung Neoplasms

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Source

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Identifiers

PMID: 42048614
DOI: 10.1158/2326-6066.CIR-25-0534
PMCID: PMC13348722

Genes

STK11
C3
CXCL2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

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Tumor-Derived Complement C3 Overexpression in STK11-Mutant Lung Adenocarcinoma Drives Tumor Growth and Immune Checkpoint Inhibitor Resistance.PMID 42048614Read ↗

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