ArticleCommunications biology2026
cPLA2α inhibition potentiates anti-PD-1 immunotherapy in lung adenocarcinoma via remodeling tumor microenvironment.
Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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16 authors.
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Abstract
Although immune checkpoint inhibitors (ICIs) against PD-1/PD-L1 have revolutionized lung adenocarcinoma (LUAD) therapy, resistance and low response rates persist. Cytoplasmic phospholipase A2α (cPLA2α), a key enzyme in inflammatory pathways, promotes tumor progression, yet its immunomodulatory role in LUAD is unclear. Here, cPLA2α overexpression is found in LUAD tissues, correlating with poor prognosis. cPLA2α knockdown inhibits lung cancer cell proliferation, migration in vitro, and tumor growth in immunodeficient mice, but efficacy diminishes in immunocompetent models due to STAT3-mediated PD-L1 upregulation. In syngeneic models, cPLA2α silencing promotes CD8
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