ArticleFrontiers in bioengineering and biotechnology2020
Proteomic Reveals Reasons for Acquired Drug Resistance in Lung Cancer Derived Brain Metastasis Based on a Newly Established Multi-Organ Microfluidic Chip Model.
Article in Frontiers in bioengineering and biotechnology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 31 citations in OpenAlex.
- Bridging Organ-on-a-Chip and Omics: A Multi-Dimensional Frontier in Biomedical Research.Biotechnology and bioengineering · 2026Review
- Organ-on-a-Chip Technology and Global Multi-Omics: Current Applications and Future Directions.MedComm · 2026Review
- CD146Theranostics · 2026Article
- The epigenetic landscape of brain metastasis.Oncogene · 2025Review
- Epithelial-to-mesenchymal transition (EMT) and cancer metastasis: the status quo of methods and experimental models 2025.Molecular cancer · 2025Review
- Review
- Mass Spectrometry-Based Applications of Spheroids in Cancer Biology.Annual review of analytical chemistry (Palo Alto, Calif.) · 2025Review
- Molecular evolution of central nervous system metastasis and therapeutic implications.Trends in molecular medicine · 2025Review
- Cancer 3D Models: Essential Tools for Understanding and Overcoming Drug Resistance.Oncology research · 2025Review
- Application and development of Organ-on-a-Chip technology in cancer therapy.Frontiers in oncology · 2025Review
- Review
- Establishment of a cholangiocarcinoma risk evaluation model based on mucin expression levels.World journal of gastrointestinal oncology · 2024Article
- 3D cell culture models in research: applications to lung cancer pharmacology.Frontiers in pharmacology · 2024Review
- Experimental models for cancer brain metastasis.Cancer pathogenesis and therapy · 2024Review
- CD146 promotes resistance of NSCLC brain metastases to pemetrexed via the NF-κB signaling pathway.Frontiers in pharmacology · 2024Article
- Radiotherapy in Preclinical Models of Brain Metastases: A Review and Recommendations for Future Studies.International journal of biological sciences · 2024Review
- Assessment of hypoxia and oxidative-related changes in a lung-derived brain metastasis model by [EJNMMI research · 2023Article
- MTX-211 Inhibits GSH Synthesis through Keap1/NRF2/GCLM Axis and Exerts Antitumor Effects in Bladder Cancer.International journal of molecular sciences · 2023Article
- Advanced lung organoids and lung-on-a-chip for cancer research and drug evaluation: a review.Frontiers in bioengineering and biotechnology · 2023Review
- Patient-derived organoids of lung cancer based on organoids-on-a-chip: enhancing clinical and translational applications.Frontiers in bioengineering and biotechnology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anti-tumor drugs can effectively shrink the lesions of primary lung cancer; however, it has limited therapeutic effect on patients with brain metastasis (BM). A BM preclinical model based on a multi-organ microfluidic chip has been established proficiently in our previous work. In this study, the BM subpopulation (PC9-Br) derived from the parental PC9 cell line was isolated from the chip model and found to develop obvious resistance to antineoplastic drugs including chemotherapeutic agents (cisplatin, carboplatin, pemetrexed) and tyrosine kinase inhibitors (TKIs) which target epidermal growth factor receptor (EGFR); this suggested that the acquisition of drug-resistance by brain metastatic cells was attributable to the intrinsic changes in PC9-Br. Hence, we performed proteomic and revealed a greatly altered spectrum of BM protein expression compared with primary lung cancer cells. We identified the hyperactive glutathione (GSH) metabolism pathway with the overexpression of various GSH metabolism-related enzymes (GPX4, RRM2, GCLC, GPX1, GSTM4, GSTM1). Aldehyde dehydrogenases (ALDH1A1, ALDH3A1) were also found to be upregulated in BM. What's more, loss of EGFR and phosphorylated EGFR in PC9-Br gave reasons for the TKIs resistance. Collectively, our findings indicated potential mechanisms for the acquirement of drug resistance occurred in BM, providing new strategies to overcome therapeutic resistance in lung cancer BM.
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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.