ArticleMolecular cancer therapeutics2018
JQ1 Induces DNA Damage and Apoptosis, and Inhibits Tumor Growth in a Patient-Derived Xenograft Model of Cholangiocarcinoma.
Article in Molecular cancer therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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
26 citing papers in PubMed, 35 citations in OpenAlex.
- Construction of PANoptosis-related LncRNA Prognostic Signature and Functional Analysis of AC034229.4 in Hepatocellular Carcinoma.Current medicinal chemistry · 2026Article
- MYC-Mediated Functional Manifestation of IDH1 Mutations in Intrahepatic Cholangiocarcinoma Confers Sensitivity to (+)-JQ1.International journal of biological sciences · 2026Article
- Preclinical evaluation of JQ1 in esophageal squamous cell carcinoma: growth and migration suppression with BRD4-associated DNA damage and apoptotic signaling.Frontiers in pharmacology · 2026Article
- [Pathology of liver tumours in animal models].Pathologie (Heidelberg, Germany) · 2025Review
- Review
- MerTK Drives Proliferation and Metastatic Potential in Triple-Negative Breast Cancer.International journal of molecular sciences · 2024Article
- Review
- Human Metastatic Cholangiocarcinoma Patient-Derived Xenografts and Tumoroids for Preclinical Drug Evaluation.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Combined inhibition of BET bromodomain and mTORC1/2 provides therapeutic advantage for rhabdomyosarcoma by switching cell death mechanism.Molecular carcinogenesis · 2022Article
- Bromodomain and extra-terminal inhibitors emerge as potential therapeutic avenues for gastrointestinal cancers.World journal of gastrointestinal oncology · 2022Review
- Overcome Drug Resistance in Cholangiocarcinoma: New Insight Into Mechanisms and Refining the Preclinical Experiment Models.Frontiers in oncology · 2022Review
- A novel BRD4 inhibitor suppresses osteoclastogenesis and ovariectomized osteoporosis by blocking RANKL-mediated MAPK and NF-κB pathways.Cell death & disease · 2021Article
- Epigenetic Treatment of Urothelial Carcinoma Cells Sensitizes to Cisplatin Chemotherapy and PARP Inhibitor Treatment.Cancers · 2021Article
- The Application Progress of Patient-Derived Tumor Xenograft Models After Cholangiocarcinoma Surgeries.Frontiers in oncology · 2021Review
- Review
- The application of histone deacetylases inhibitors in glioblastoma.Journal of experimental & clinical cancer research : CR · 2020Review
- In Vivo Models for Cholangiocarcinoma-What Can We Learn for Human Disease?International journal of molecular sciences · 2020Review
- Article
- BRD4 inhibition exerts anti-viral activity through DNA damage-dependent innate immune responses.PLoS pathogens · 2020Article
- Applications of patient-derived tumor xenograft models and tumor organoids.Journal of hematology & oncology · 2020Review
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
Cholangiocarcinoma (CCA) is a fatal disease with a 5-year survival of <30%. For a majority of patients, chemotherapy is the only therapeutic option, and virtually all patients relapse. Gemcitabine is the first-line agent for treatment of CCA. Patients treated with gemcitabine monotherapy survive ∼8 months. Combining this agent with cisplatin increases survival by ∼3 months, but neither regimen produces durable remissions. The molecular etiology of this disease is poorly understood. To facilitate molecular characterization and development of effective therapies for CCA, we established a panel of patient-derived xenograft (PDX) models of CCA. We used two of these models to investigate the antitumor efficacy and mechanism of action of the bromodomain inhibitor JQ1, an agent that has not been evaluated for the treatment of CCA. The data show that JQ1 suppressed the growth of the CCA PDX model CCA2 and demonstrate that growth suppression was concomitant with inhibition of c-Myc protein expression. A second model (CCA1) was JQ1-insensitive, with tumor progression and c-Myc expression unaffected by exposure to this agent. Also selective to CCA2 tumors, JQ1 induced DNA damage and apoptosis and downregulated multiple c-Myc transcriptional targets that regulate cell-cycle progression and DNA repair. These findings suggest that c-Myc inhibition and several of its transcriptional targets may contribute to the mechanism of action of JQ1 in this tumor type. We conclude that BET inhibitors such as JQ1 warrant further investigation for the treatment of CCA.
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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.