ArticleScientific reports2019
Continuous targeted kinase inhibitors treatment induces upregulation of PD-L1 in resistant NSCLC.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 44 citations in OpenAlex.
- A clinical decision framework for redox-adapted, EMT-high cancers: From ferroptosis resistance to precision therapeutic stratification.Redox biology · 2026Review
- Association of CMTM6 expression with clinicopathological characteristics and prognostic implications in renal cell carcinoma.Therapeutic advances in medical oncology · 2026Article
- Immunomodulation on tumor immune microenvironment in acquired targeted therapy resistance and implication for immunotherapy resistance.Translational oncology · 2025Review
- Machine learning identifies clinical tumor mutation landscape pathways of resistance to checkpoint inhibitor therapy in NSCLC.Journal for immunotherapy of cancer · 2025Article
- Targeting the Tumor Microenvironment in EGFR-Mutant Lung Cancer: Opportunities and Challenges.Biomedicines · 2025Review
- Investigating subregional PD-L1 expression within primary tumors to predict clinical outcomes in advanced NSCLC patients who received ICB-based therapy.Frontiers in oncology · 2025Article
- Cytochalasin H enhances sensitivity to gefitinib in non-small-cell lung cancer cells through inhibiting EGFR activation and PD-L1 expression.Scientific reports · 2024Article
- Prognostic significance and response to immune checkpoint inhibitors of RIPK3, MLKL and necroptosis in non-small cell lung cancer.Scientific reports · 2024Article
- Upregulation of Immune checkpoint PD-L1 in Colon cancer cell lines and activation of T cells by Leuconostoc mesenteroides.World journal of microbiology & biotechnology · 2024Article
- Progress of immune checkpoint inhibitors therapy for non-small cell lung cancer with liver metastases.British journal of cancer · 2024Review
- Acetylation increases expression, interaction with TRAPPC4 and surface localization of PD-L1.Discover oncology · 2023Article
- Changes of tumor microenvironment in non-small cell lung cancer after TKI treatments.Frontiers in immunology · 2023Review
- Molecular pathways, resistance mechanisms and targeted interventions in non-small-cell lung cancer.Molecular biomedicine · 2022Review
- [Advances in ICIs Therapy after TKIs Resistance in Patients with EGFR Mutant NSCLC: A Review].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2022Review
- Immunological effect of tyrosine kinase inhibitors on the tumor immune environment in non-small cell lung cancer.Oncology letters · 2022Review
- Improvement of the anticancer efficacy of PD-1/PD-L1 blockade via combination therapy and PD-L1 regulation.Journal of hematology & oncology · 2022Review
- Molecular Pathology of Lung Cancer.Cold Spring Harbor perspectives in medicine · 2022Review
- Comprehensive Molecular Landscape of Cetuximab Resistance in Head and Neck Cancer Cell Lines.Cells · 2022Article
- A novel C-terminal heat shock protein 90 inhibitor that overcomes STAT3-Wnt-β-catenin signaling-mediated drug resistance and adverse effects.Theranostics · 2022Article
- Choosing the optimal immunotherapeutic strategies for non-small cell lung cancer based on clinical factors.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
First-generation epidermal growth factor receptor (EGFR) targeted kinase inhibitors (TKIs) are still used in selected non-small cell lung cancer (NSCLC) patients despite the resistance. Based on the correlation of programmed cell death receptor ligand 1 (PD-L1) and EGFR signaling pathway, whether continuous TKIs treatment will affect PD-L1 expression after disease progression remains unclear. To investigate the potential change of PD-L1 expression in TKI-resistant NSCLC after continuous TKIs treatment, we treated H1975 and HCC827 for more than one month and explored the possible effect on immune cells as well as underlying biological mechanisms. We found that continuous exposure to TKIs induced upregulation of PD-L1 in H1975 and HCC827. Moreover, PD-L1 upregulation significantly inhibited proliferation and slightly promoted apoptosis of T cells. We observed the activation of STAT3 and ERK1/2 along with the PD-L1 upregulation. With the pathway inhibitors, we found ERK1/2 pathway involved in inducing PD-L1 in resistant lung cancer. This study provides preclinical evidence that continuous TKIs treatment may induce PD-L1 expression in resistant NSCLC, resulting in the suppression of T cell function and immune escape. ERK1/2 pathway inhibitors, PD-L1/PD-1 inhibitors or combination strategies should be considered to reverse the resistance to TKIs in NSCLC patients.
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