ArticlePloS one2017
Cisplatin resistance in non-small cell lung cancer cells is associated with an abrogation of cisplatin-induced G2/M cell cycle arrest.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed, 169 citations in OpenAlex.
- A comprehensive review on apoptotic miRNAs and antagomiRs in breast cancer: Enhancing radio sensitization.Genes & diseases · 2026Review
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- Spatial transcriptomics and single-cell analyses reveal the role of the cisplatin-resistant gene panel in NSCLC progression and the tumor microenvironment, identifying LOXL2 as a potential therapeutic target.Cancer cell international · 2026Article
- Anticancer Activity of 2,3'-Dihydroxy-5'-Methoxystilbene Against NSCLC Cell Lines Through AKT-Dependent Mechanisms: A Comprehensive In Vitro and Computational Analysis.International journal of molecular sciences · 2026Article
- GATOR1 complex controls cisplatin sensitivity.Cell death & disease · 2025Article
- Dose-dependent effects of wheat germ oil and vitamin E on apoptosis and gene expression in breast and cervical cancer cell lines with single-cell RNA-seq profiling.Scientific reports · 2025Article
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- From mitochondrial DNA arrangement to repair: a kinetoplast-associated protein with different roles in two trypanosomatid species.Parasites & vectors · 2025Article
- Drug-Resistant Cholangiocarcinoma Cell Lines for Therapeutic Evaluation of Novel Drugs.Molecules (Basel, Switzerland) · 2025Article
- Circular RNA rising star: new findings of circPRMT5 in cancer.Molecular biology reports · 2025Review
- Extracts fromMarine drugs · 2025Article
- Tanshinone II A Facilitates Chemosensitivity of Osteosarcoma Cells to Cisplatin via Activation of p38 MAPK Pathway.Chinese journal of integrative medicine · 2025Article
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- The potential of the South African plant Tulbaghia Violacea Harv for the treatment of triple negative breast cancer.Scientific reports · 2025Article
- Tumor Cell Spatial Organization Directs EGFR/RAS/RAF Pathway Primary Therapy Resistance through YAP Signaling.bioRxiv : the preprint server for biology · 2025Article
- The regulatory role of lncRNA in tumor drug resistance: refracting light through a narrow aperture.Oncology research · 2025Review
- Non-coding RNAs as potential mediators of resistance to lung cancer immunotherapy and chemotherapy.Oncology research · 2025Review
- Differential effect of targeting cisplatin-induced nitrative stress using MnTBAP in auditory and cancer cells.Current research in toxicology · 2025Article
- The Impact of Genetic Mutations on the Efficacy of Immunotherapies in Lung Cancer.International journal of molecular sciences · 2024Review
30 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The efficacy of cisplatin-based chemotherapy in cancer is limited by the occurrence of innate and acquired drug resistance. In order to better understand the mechanisms underlying acquired cisplatin resistance, we have compared the adenocarcinoma-derived non-small cell lung cancer (NSCLC) cell line A549 and its cisplatin-resistant sub-line A549rCDDP2000 with regard to cisplatin resistance mechanisms including cellular platinum accumulation, DNA-adduct formation, cell cycle alterations, apoptosis induction and activation of key players of DNA damage response. In A549rCDDP2000 cells, a cisplatin-induced G2/M cell cycle arrest was lacking and apoptosis was reduced compared to A549 cells, although equitoxic cisplatin concentrations resulted in comparable platinum-DNA adduct levels. These differences were accompanied by changes in the expression of proteins involved in DNA damage response. In A549 cells, cisplatin exposure led to a significantly higher expression of genes coding for proteins mediating G2/M arrest and apoptosis (mouse double minute 2 homolog (MDM2), xeroderma pigmentosum complementation group C (XPC), stress inducible protein (SIP) and p21) compared to resistant cells. This was underlined by significantly higher protein levels of phosphorylated Ataxia telangiectasia mutated (pAtm) and p53 in A549 cells compared to their respective untreated control. The results were compiled in a preliminary model of resistance-associated signaling alterations. In conclusion, these findings suggest that acquired resistance of NSCLC cells against cisplatin is the consequence of altered signaling leading to reduced G2/M cell cycle arrest and apoptosis.
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