ArticleMolecular cancer2017
BAP1 dependent expression of long non-coding RNA NEAT-1 contributes to sensitivity to gemcitabine in cholangiocarcinoma.
Article in Molecular cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 79 citations in OpenAlex.
- Research progress on the regulation of mesothelioma driven by deubiquitinating enzyme BAP1.Clinical and experimental medicine · 2026Review
- Functional characterization of BAP1 mutations in genome edited cholangiocarcinoma organoids: Role in cell death and drug responses.iScience · 2026Article
- Pivotal role of long non-coding RNA in the development of new therapeutic approaches for plural mesothelioma.Discover oncology · 2026Review
- The functions of circular RNAs and long noncoding RNAs in cholangiocarcinoma.Discover oncology · 2025Review
- Establishment and genomic profiling of cholangiocarcinoma cells with functional characterization.Scientific reports · 2025Article
- LINC00667: A Novel Vital Oncogenic LincRNA.Current medicinal chemistry · 2025Review
- Feedback loop LINC00511-YTHDF2-SOX2 regulatory network drives cholangiocarcinoma progression and stemness.MedComm · 2024Article
- Single-Cell Transcriptome Reveals Cell Type-Specific Molecular Pathology in a 2VO Cerebral Ischemic Mouse Model.Molecular neurobiology · 2024Article
- Current and Future Therapeutic Targets for Directed Molecular Therapies in Cholangiocarcinoma.Cancers · 2024Review
- Non-coding RNA and Drug resistance in cholangiocarcinoma.Non-coding RNA research · 2024Review
- Integration of Transcriptomics Data and Metabolomic Data Using Biomedical Literature Mining and Pathway Analysis.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Long Non-Coding RNAs as Molecular Biomarkers in Cholangiocarcinoma.Frontiers in cell and developmental biology · 2022Review
- Overcome Drug Resistance in Cholangiocarcinoma: New Insight Into Mechanisms and Refining the Preclinical Experiment Models.Frontiers in oncology · 2022Review
- Sulfasalazine modifies metabolic profiles and enhances cisplatin chemosensitivity on cholangiocarcinoma cells in in vitro and in vivo models.Cancer & metabolism · 2021Article
- Association between metformin medication, genetic variation and prostate cancer risk.Prostate cancer and prostatic diseases · 2021Article
- Long non-coding RNA LINC00665 promotes gemcitabine resistance of Cholangiocarcinoma cells via regulating EMT and stemness properties through miR-424-5p/BCL9L axis.Cell death & disease · 2021Article
- Biliary Tract Cancers: Treatment Updates and Future Directions in the Era of Precision Medicine and Immuno-Oncology.Frontiers in oncology · 2021Review
- Evolving Landscape of Long Non-coding RNAs in Cerebrospinal Fluid: A Key Role From Diagnosis to Therapy in Brain Tumors.Frontiers in cell and developmental biology · 2021Review
- Downregulation of NEAT1 sensitizes gemcitabine-resistant pancreatic cancer cells to gemcitabine through modulation of the miR-506-3p/ZEB2/EMT axis.American journal of cancer research · 2021Article
- An omics perspective on drug target discovery platforms.Briefings in bioinformatics · 2020Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundGenetic alterations in chromatin modulators such as BRCA-1 associated protein-1 (BAP1) are the most frequent genetic alteration in intrahepatic cholangiocarcinomas (CCA). We evaluated the contribution of BAP1 expression on tumor cell behavior and therapeutic sensitivity to identify rationale therapeutic strategies.
methodsThe impact of BAP1 expression on sensitivity to therapeutic agents was evaluated in CCA cells with a 7-fold difference in BAP1 expression (KMBC-low, HuCCT1-high) and genetically engineered haplo-insufficient BAP1 knockout cells. We also identified long non-coding RNA genes associated with loss of BAP1 and their role in therapeutic sensitivity.
resultsSensitivity to gemcitabine was greater in low BAP1 expressing or BAP1 knockout cells compared with the high BAP1 expressing cells or control haplo-insufficient cells respectively. Similar results were observed with TSA, olaparib, b-AP15 but not with GSK126. A differential synergistic effect was observed in combinations of gemcitabine with olaparib or GSK126 in KMBC cells and TSA or bAP15 in HuCCT1 cells, indicating BAP1 dependent target-specific synergism and sensitivity to gemcitabine. A BAP1 dependent alteration in expression of lncRNA NEAT-1 was identified by RT-PCR based lncRNA expression profiling, and an inverse relationship between this lncRNA and BAP1 was observed in analysis of the Tumor Cancer Genome Atlas cholangiocarcinoma dataset. Exogenous modulation of NEAT-1 and/or BAP1 expression altered tumor cell phenotype and modulated sensitivity to gemcitabine.
conclusionsNEAT-1 is a downstream effector of gemcitabine sensitivity in CCA. The expression of BAP1 is a determinant of sensitivity to therapeutic drugs that can be exploited to enhance responses through combination strategies.
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