ArticleThe FEBS journal2025
The G protein-coupled receptor GPR89A is a novel potential therapeutic target to overcome cisplatin resistance in NSCLC Calu1 cells.
Article in The FEBS journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Metabolomic Analysis of Intracellular Amino Acid Profile Differences Between Cisplatin-Resistant and Cisplatin- Sensitive CALU-1 Lung Cancer Cells.Cell biochemistry and biophysics · 2026Article
- Toll-Like Receptors in Diabetes: Immunometabolic Mechanisms and Emerging Precision Therapeutic Strategies.Journal of inflammation research · 2026Review
- Evolutionary and structural bioinformatics identifies GPR89 as a conserved member of the LIMR protein superfamily.Computational and structural biotechnology journal · 2025Article
- miR-199a-5p/GPR89A axis modulates sorafenib resistance in hepatocellular carcinoma through glutamate metabolic reprogramming.Science progressArticle
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Lung cancer is the most frequently diagnosed cancer type worldwide and is characterised by its high metastatic potential. Standard therapy for nonsmall cell lung cancer (NSCLC) cases includes chemotherapy with the platinum-based chemotherapeutic agent cisplatin. Although lung cancer cases respond well to cisplatin at the beginning of treatment, ~ 60% develop chemotherapy resistance during this process. In this study, a genome-wide CRISPR-Cas9-based genetic screening approach was employed to identify genes that cisplatin-resistant NSCLC Calu1 cells are more addicted to than sensitive cells. Cisplatin-resistant Calu1 cells were generated by the dose escalation method, and genome-wide CRISPR-Cas9-based genetic screening was performed with the Brunello CRISPR knockout library. Bioinformatics analyses of the obtained next-generation sequencing data revealed 63 potential candidate genes responsible for cisplatin resistance, including G protein-coupled receptor 89A (GPR89A), Poly(U) binding splicing factor 60 (PUF60), NBAS subunit of NRZ tethering complex (NBAS) and GrpE like 1, mitochondrial (GRPEL1). The GPR89A protein is located in the Golgi cisterna and Golgi-associated vesicle membrane, enables voltage-gated anion channel activity, and is involved in intracellular pH reduction. Functional studies carried out with GPR89A-knockout cisplatin-resistant Calu1 cells resulted in cell cycle arrest in the G2/M phase and increased polyploidy, and also prevented colony formation and cell migration. Cisplatin treatment, on the other hand, resulted in increased cell death by apoptosis upon cell cycle arrest in the S phase. In conclusion, this is the first study that identified GPR89A as a potential therapeutic target to overcome cisplatin resistance in NSCLC Calu1 cells.
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Registered trials
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