ArticleOncotarget2018
PD-L1 confers resistance to EGFR mutation-independent tyrosine kinase inhibitors in non-small cell lung cancer via upregulation of YAP1 expression.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- Reactive oxygen species drive wound epithelium and blastema formation in regenerating tail of Scincella tsinlingensis.Frontiers in zoology · 2026Article
- Drug resistant cancer cells show increased nuclear mechanotransduction and mechanically targetable YAP-regulated vulnerability.Biomaterials · 2026Article
- Anti-PD-1/PD-L1 Immunotherapy as a Potential Treatment Option for Lung Cancer: A Perspective Analysis of Opportunities and Challenges.Health science reports · 2026Article
- Restoring osimertinib sensitivity in EGFR-mutant NSCLC: the role of anlotinib in modulating Wnt/β-catenin/YAP pathways.American journal of cancer research · 2026Article
- Ramucirumab and erlotinib combination as first-line treatment for advanced or recurrent non-small cell lung cancer harboringTherapeutic advances in medical oncology · 2025Article
- Hippo pathway in non-small cell lung cancer: mechanisms, potential targets, and biomarkers.Cancer gene therapy · 2024Review
- Oxidative stress in pituitary neuroendocrine tumors: Affecting the tumor microenvironment and becoming a new target for pituitary neuroendocrine tumor therapy.CNS neuroscience & therapeutics · 2023Review
- Insights into recent findings and clinical application of YAP and TAZ in cancer.Nature reviews. Cancer · 2023Review
- First-line osimertinib for patients with EGFR-mutated advanced non-small cell lung cancer: efficacy and safety during the COVID-19 pandemic.Translational lung cancer research · 2023Article
- Alteration of Mesenchymal Stem Cells Isolated from Glioblastoma Multiforme under the Influence of Photodynamic Treatment.Current issues in molecular biology · 2023Article
- Comprehensive analysis and molecular map of Hippo signaling pathway in lower grade glioma: the perspective toward immune microenvironment and prognosis.Frontiers in oncology · 2023Article
- YAP1 synergize with YY1 transcriptional co-repress DUSP1 to induce osimertinib resistant by activating the EGFR/MAPK pathway and abrogating autophagy in non-small cell lung cancer.International journal of biological sciences · 2023Article
- Optimizing the clinical management ofTranslational lung cancer research · 2022Review
- Molecular profile of pure squamous cell carcinoma of the bladder identifies major roles for OSMR and YAP signalling.The journal of pathology. Clinical research · 2022Article
- High dimensionality reduction by matrix factorization for systems pharmacology.Briefings in bioinformatics · 2022Article
- A narrative review for the Hippo-YAP pathway in cancer survival and immunity: the Yin-Yang dynamics.Translational cancer research · 2022Review
- Self-Sustained Regulation or Self-Perpetuating Dysregulation: ROS-dependent HIF-YAP-Notch Signaling as a Double-Edged Sword on Stem Cell Physiology and Tumorigenesis.Frontiers in cell and developmental biology · 2022Review
- Post-amputation reactive oxygen species production is necessary for axolotls limb regeneration.Frontiers in cell and developmental biology · 2022Article
- YAP/Hippo Pathway and Cancer Immunity: It Takes Two to Tango.Biomedicines · 2021Review
- Alantolactone is a natural product that potently inhibits YAP1/TAZ through promotion of reactive oxygen species accumulation.Cancer science · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Programmed death ligand (PD-L1) expression was associated with tumor immune escape and subsequent poor prognosis in non-small cell lung cancer (NSCLC). This expression was higher in patients with EGFR-mutated NSCLC tumors than in those with EGFR-wild-type (WT) NSCLC tumors. We therefore hypothesized that poor prognosis mediated by higher PD-L1 may be partially through conferring resistance to tyrosine kinase inhibitor (TKI) in NSCLC regardless of EGFR mutation. The change in PD-L1 expression following gene manipulation corresponded with changes in expression of HIF-1α and YAP1. The expression of HIF-1α and YAP1 was concomitantly decreased by PD-L1 silencing or by ROS scavenger treatment (N-acetylcysteine, NAC); however, a ROS inducer treatment (pyocyanin) completely reversed the decreased expression of both genes in EGFR-mutated and -wild-type (WT) NSCLC cells. The MTT assay indicated that the inhibitory concentration of gefitinib yielding 50% cell viability (IC50) depended on PD-L1-mediated YAP1 expression. Mechanistic studies indicated that upregulation of YAP1 by PD-L1 might be responsible for EGFR mutation-independent TKI resistance via the ROS/HIF-1α axis. An unfavorable TKI response was more common in patient tumors with high PD-L1 or YAP1 mRNA expression than in patient tumors with low mRNA expression of these genes. In conclusion, PD-L1 might confer EGFR mutation-independent TKI resistance in NSCLC cells via upregulation of YAP1 expression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.