ArticleCancer letters2018
Integrated proteomic and phosphoproteomic analyses of cisplatin-sensitive and resistant bladder cancer cells reveal CDK2 network as a key therapeutic target.
Article in Cancer letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- A cyclin D1-CDK4/6-E2F dependency represents an acquired vulnerability in cisplatin-resistant bladder cancer.Biology direct · 2026Article
- Polyploidy in Cancer: Causal Mechanisms, Cancer-Specific Consequences, and Emerging Treatments.Molecular cancer therapeutics · 2024Review
- [Procine recombinant NK-lysin inhibits hepatocellular carcinoma metastasis by downregulating FKBP3 and inhibiting oxidative phosphorylation and glycolysis: a proteomic analysis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Cisplatin-Resistant Ovarian Cancer Cells Reveal a Polyploid Phenotype with Remarkable Activation of Nuclear Processes.Advanced biomedical research · 2023Article
- A review on the role of cyclin dependent kinases in cancers.Cancer cell international · 2022Review
- Allyl-, Butyl- and Phenylethyl-Isothiocyanate Modulate Akt-mTOR and Cyclin-CDK Signaling in Gemcitabine- and Cisplatin-Resistant Bladder Cancer Cell Lines.International journal of molecular sciences · 2022Article
- Quantitative proteomics characterization of cancer biomarkers and treatment.Molecular therapy oncolytics · 2021Review
- Pharmacological Inhibition of miR-130 Family Suppresses Bladder Tumor Growth by Targeting Various Oncogenic Pathways via PTPN1.International journal of molecular sciences · 2021Article
- Proteomics and phosphoproteomics reveal key regulators associated with cytostatic effect of amino acid transporter LAT1 inhibitor.Cancer science · 2021Article
- Circulating proteomic signature for detection of biomarkers in bladder cancer patients.Scientific reports · 2020Article
- Mechanisms behind Temsirolimus Resistance Causing Reactivated Growth and Invasive Behavior of Bladder Cancer Cells In Vitro.Cancers · 2019Article
- Spermine modified polymeric micelles with pH-sensitive drug release for targeted and enhanced antitumor therapy.RSC advances · 2019Article
- Elucidation of the Mechanism of Action for Metal Based Anticancer Drugs by Mass Spectrometry-Based Quantitative Proteomics.Molecules (Basel, Switzerland) · 2019Review
- Centromere protein F (CENPF), a microtubule binding protein, modulates cancer metabolism by regulating pyruvate kinase M2 phosphorylation signaling.Cell cycle (Georgetown, Tex.) · 2018Article
- Bladder Cancer-related microRNAs With In Vivo Efficacy in Preclinical Models.Cancer diagnosis & prognosisReview
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundCisplatin-based chemotherapy is currently part of the standard of care for bladder cancer (BC). Unfortunately, some patients respond poorly to chemotherapy and have acquired or developed resistance. The molecular mechanisms underlying this resistance remain unclear. Here, we introduce a multidimensional proteomic analysis of a cisplatin-resistant BC model that provides different levels of protein information, including that of the global proteome and phosphoproteome.
methodsTo characterize the global proteome and phosphoproteome in cisplatin-resistant BC cells, liquid chromatography-mass spectrometry/mass spectrometry experiments combined with comprehensive bioinformatics analysis were performed. Perturbed expression and phosphorylation levels of key kinases associated with cisplatin resistance were further studied using various cell biology assays, including western blot analysis.
resultsAnalyses of protein expression and phosphorylation identified significantly altered proteins, which were also EGF-dependent and independent. This suggests that protein phosphorylation plays a significant role in cisplatin-resistant BC. Additional network analysis of significantly altered proteins revealed CDK2, CHEK1, and ERBB2 as central regulators mediating cisplatin resistance. In addition to this, we identified the CDK2 network, which consists of CDK2 and its 5 substrates, as being significantly associated with poor survival after cisplatin chemotherapy.
conclusionsCollectively, these findings potentially provide a novel way of classifying higher-risk patients and may guide future research in developing therapeutic targets.
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