ArticlePloS one2010
High-definition DNA methylation profiles from breast and ovarian carcinoma cell lines with differing doxorubicin resistance.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 32 citations in OpenAlex.
- Araçá-Boi Extract and Gallic Acid Reduce Cell Viability and Modify the Expression of Tumor Suppressor Genes and Genes Involved in Epigenetic Processes in Ovarian Cancer.Plants (Basel, Switzerland) · 2025Article
- Exploring miRNA profile associated with cisplatin resistance in ovarian cancer cells.Biochemistry and biophysics reports · 2025Article
- Cancer chemoresistance and its mechanisms: Associated molecular factors and its regulatory role.Medical oncology (Northwood, London, England) · 2023Review
- The role of DNA methylation in ovarian cancer chemoresistance: A narrative review.Health science reports · 2023Article
- Investigation of role of CpG methylation in some epithelial mesenchymal transition gene in a chemoresistant ovarian cancer cell line.Scientific reports · 2022Article
- Development and application of novel BiFC probes for cell sorting based on epigenetic modification.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2022Article
- Predictive value of unmethylated RASSF1A on disease progression in non-small cell lung cancer patients receiving pemetrexed-based chemotherapy.Cancer biomarkers : section A of Disease markers · 2020Article
- Article
- Nanogel-mediated delivery of a cocktail of epigenetic drugs plus doxorubicin overcomes drug resistance in breast cancer cells.Drug delivery and translational research · 2018Article
- ETV7-Mediated DNAJC15 Repression Leads to Doxorubicin Resistance in Breast Cancer Cells.Neoplasia (New York, N.Y.) · 2018Article
- Chaperoning mitochondrial permeability transition: regulation of transition pore complex by a J-protein, DnaJC15.Cell death & disease · 2014Article
- Multidrug-resistant breast cancer: current perspectives.Breast cancer (Dove Medical Press) · 2014Review
- Review
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Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acquired drug resistance represents a frequent obstacle which hampers efficient chemotherapy of cancers. The contribution of aberrant DNA methylation to the development of drug resistant tumor cells has gained increasing attention over the past decades. Hence, the objective of the presented study was to characterize DNA methylation changes which arise from treatment of tumor cells with the chemotherapeutic drug doxorubicin. DNA methylation levels from CpG islands (CGIs) linked to twenty-eight genes, whose expression levels had previously been shown to contribute to resistance against DNA double strand break inducing drugs or tumor progression in different cancer types were analyzed. High-definition DNA methylation profiles which consisted of methylation levels from 800 CpG sites mapping to CGIs around the transcription start sites of the selected genes were determined. In order to investigate the influence of CGI methylation on the expression of associated genes, their mRNA levels were investigated via qRT-PCR. It was shown that the employed method is suitable for providing highly accurate methylation profiles, comparable to those obtained via clone sequencing, the gold standard for high-definition DNA methylation studies. In breast carcinoma cells with acquired resistance against the double strand break inducing drug doxorubicin, changes in methylation of specific cytosines from CGIs linked to thirteen genes were detected. Moreover, similarities between methylation profiles obtained from breast and ovarian carcinoma cell lines with acquired doxorubicin resistance were found. The expression levels of a subset of analyzed genes were shown to be linked to the methylation levels of the analyzed CGIs. Our results provide detailed DNA methylation information from two separate model systems for acquired doxorubicin resistance and suggest the occurrence of similar methylation changes in both systems upon exposure to the drug.
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