ArticleOncotarget2016
ATR-Chk1 signaling inhibition as a therapeutic strategy to enhance cisplatin chemosensitivity in urothelial bladder cancer.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 30 citations in OpenAlex.
- ATR inhibitors synergise with mitomycin C to enhance cytotoxicity in patient-derived non-muscle invasive bladder cancer organoids.British journal of cancer · 2026Article
- Exploring the Chemical Space Around Protoflavonoids: Synthesis and Antitumor Activity of Protochalcones.ChemMedChem · 2026Article
- Regulation of drug resistance in bladder urothelial carcinoma by tumor aerobic glycolysis.Journal of translational medicine · 2025Review
- Lysine demethylase 5D promotes CHEK1 inhibitor sensitivity through p38-mediated cyclooxygenase-2 expression in castration-resistant prostate cancer cells.The Journal of pharmacology and experimental therapeutics · 2025Article
- Synthesis and anti-cancer biological evaluation of a novel protoapigenone analogue, WYC-241.RSC medicinal chemistry · 2025Article
- Synthetic Lethality-Based Targets and Their Exploration in Tumour Combination Strategies.Journal of cellular and molecular medicine · 2025Review
- Embryonic Stem Cell-Specific Responses to DNA Replication Stress.bioRxiv : the preprint server for biology · 2025Article
- Enhanced pharmacological activities of AKR1C3-activated prodrug AST-3424 in cancer cells with defective DNA repair.International journal of cancer · 2025Article
- Studying the DNA damage response pathway in hematopoietic canine cancer cell lines, a necessary step for finding targets to generate new therapies to treat cancer in dogs.Frontiers in veterinary science · 2023Article
- Natural products targeting the ATR-CHK1 signaling pathway in cancer therapy.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Hydrogen Sulfide Biology and Its Role in Cancer.Molecules (Basel, Switzerland) · 2022Review
- Ataxia telangiectasia and Rad3-related inhibition by AZD6738 enhances gemcitabine-induced cytotoxic effects in bladder cancer cells.PloS one · 2022Article
- Bad Smells and Broken DNA: A Tale of Sulfur-Nucleic Acid Cooperation.Antioxidants (Basel, Switzerland) · 2021Review
- Molecular Functions of Hydrogen Sulfide in Cancer.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021Review
- Inhibition of checkpoint kinase 1 potentiates anticancer activity of gemcitabine in bladder cancer cells.Scientific reports · 2021Article
- CDKN1A/p21American journal of cancer research · 2021Article
- Phosphatase POPX2 interferes with cell cycle by interacting with Chk1.Cell cycle (Georgetown, Tex.) · 2020Article
- Predictive and Prognostic Value of DNA Damage Response Associated Kinases in Solid Tumors.Frontiers in oncology · 2020Review
- Therapeutic Targeting of the DNA Damage Response Using an ATR Inhibitor in Biliary Tract Cancer.Cancer research and treatment · 2019Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA damage responses contribute to cisplatin resistance; however, therapeutic strategies to overcome cisplatin resistance have not yet been established. Here, we demonstrate that inhibition of ATR-Chk1 pathway with the potent inhibitor WYC0209 sensitizes bladder cancer cells to cisplatin. In the clinical microarray profile, high ATR expression is associated with poor prognosis in bladder cancer patients who receive chemotherapy. We show that pharmacological and genetic suppressing of ATR sensitized cells to cisplatin. Treatment with WYC0209 or siATR increased levels of cisplatin-DNA adducts, concomitant with decreased levels of p-glycoprotein expression. Additionally, Combinations of cisplatin and WYC0209 show synergistic activity against bladder cancer. Ultimately, WYC0209 enhanced the anti-tumor effects of cisplatin and suppressed p-glycoprotein expression in bladder cancer xenografts. These results indicate that inhibiting ATR-Chk1 activation with WYC0209 suppresses p-glycoprotein expression and increases cisplatin activity in bladder cancer. Our findings collectively suggest that ATR-Chk1 is a target for improving the efficacy of cisplatin in bladder cancer.
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Registered trials
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.