ArticleMolecular pharmacology2014
Reversible epigenetic regulation of 14-3-3σ expression in acquired gemcitabine resistance by uhrf1 and DNA methyltransferase 1.
Article in Molecular pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Novel quinoxaline-based survivin degraders overcome docetaxel-resistance in castration-resistant prostate cancer.Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy · 2026Review
- Transfer learning with multiomics integration and deep neural networks reveals drug resistance mechanisms in cancer.Scientific reports · 2025Article
- Role and clinical significance of the DNA methylation of 14-3-3σ in cancer (Review).Oncology letters · 2025Review
- Planar cell polarity geneEMBO reports · 2018Article
- Targeting microRNA/UHRF1 pathways as a novel strategy for cancer therapy.Oncology letters · 2018Article
- The epigenetic integrator UHRF1: on the road to become a universal biomarker for cancer.Oncotarget · 2017Review
- 14-3-3σ Contributes to Radioresistance By Regulating DNA Repair and Cell Cycle via PARP1 and CHK2.Molecular cancer research : MCR · 2017Article
- Hypomethylating agents synergize with irinotecan to improve response to chemotherapy in colorectal cancer cells.PloS one · 2017Article
- The histone methyltransferase G9a as a therapeutic target to override gemcitabine resistance in pancreatic cancer.Oncotarget · 2016Article
- 14-3-3σ regulation of and interaction with YAP1 in acquired gemcitabine resistance via promoting ribonucleotide reductase expression.Oncotarget · 2016Article
- Genomic analysis of drug resistant pancreatic cancer cell line by combining long non-coding RNA and mRNA expression profling.International journal of clinical and experimental pathology · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Although gemcitabine is the most commonly used drug for treating pancreatic cancers, acquired gemcitabine resistance in a substantial number of patients appears to hinder its effectiveness in successful treatment of this dreadful disease. To understand acquired gemcitabine resistance, we generated a gemcitabine-resistant pancreatic cancer cell line using stepwise selection and found that, in addition to the known mechanisms of upregulated expression of ribonucleotide reductase, 14-3-3σ expression is dramatically upregulated, and that 14-3-3σ overexpression contributes to the acquired resistance to gemcitabine and cross-resistance to cytarabine. We also found that the increased 14-3-3σ expression in the gemcitabine-resistant cells is due to demethylation of the 14-3-3σ gene during gemcitabine selection, which could be partially reversed with removal of the gemcitabine selection pressure. Most importantly, the reversible methylation/demethylation of the 14-3-3σ gene appears to be carried out by DNA methyltransferase 1 under regulation by Uhrf1. These findings suggest that the epigenetic regulation of gene expression may play an important role in gemcitabine resistance, and that epigenetic modification is reversible in response to gemcitabine treatment.
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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.