ArticleCancer science2025
Intrinsic PDL1 Signaling Modulates TGFBI-Mediated Growth Suppression in Lung Adenocarcinoma.
Article in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Identification and functional validation of EPS15L1 as a key driver of triple-negative breast cancer.NPJ breast cancer · 2026Article
- TGFBI in tumors and the tumor immune microenvironment: functional roles, mechanisms, and therapeutic targeting.Frontiers in immunology · 2026Review
- Application value of a prognostic risk model based on lactate-related genes in non-small cell lung cancer.Translational cancer research · 2025Article
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Authors and funding
7 authors.
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Abstract
Programmed death ligand 1 (PDL1) suppresses T-cell immunity by engaging programmed cell death protein 1 (PD1), and its blockade can activate T-cell responses. Although PDL1 is a transmembrane protein, its intrinsic signaling role in regulating oncogenesis remains unclear. Our study reveals lung adenocarcinomas (ADCs) exhibit deficient PDL1 expression, which correlates with poor patient prognosis. TGF-β stimulation induced PDL1 expression, while silencing PDL1 in PDL1-high lung ADC cells enhanced colony formation, and PDL1 overexpression inhibited lung cancer cell growth. Cell cycle analysis indicated that PDL1 silencing increased S-phase entry in lung ADC cells. Furthermore, PDL1 expression reduced FAK, ERK, and AKT phosphorylation, increasing cell detachment from the substrate. Gene expression profiling identified TGFBI as a downstream molecule of PDL1. TGF-β induced TGFBI expression, and knockdown of TGFBI increased the growth of lung ADC cells. Given that TGF-β regulates CITED2 and p21
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