ArticleDrug design, development and therapy2015
MicroRNA-133b targets glutathione S-transferase π expression to increase ovarian cancer cell sensitivity to chemotherapy drugs.
Article in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 70 citations in OpenAlex.
- Article
- Targeting epigenetic networks to overcome cisplatin resistance in ovarian cancer: from mechanisms to clinical translation.Journal of ovarian research · 2026Review
- MiRNAs: main players of cancer drug resistance target ABC transporters.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Therapeutic Chemoresistance in Ovarian Cancer: Emerging Hallmarks, Signaling Mechanisms and Alternative Pathways.Current medicinal chemistry · 2025Review
- Molecular mechanisms of cisplatin resistance in ovarian cancer.Genes & diseases · 2024Review
- Role of microRNAs in regulation of doxorubicin and paclitaxel responses in lung tumor cells.Cell division · 2023Review
- Natural Compounds and Glutathione: Beyond Mere Antioxidants.Antioxidants (Basel, Switzerland) · 2023Review
- Research progress of circulating non-coding RNA in diagnosis and treatment of hepatocellular carcinoma.Frontiers in oncology · 2023Review
- Glutathione Transferase P1: Potential Therapeutic Target in Ovarian Cancer.Medicina (Kaunas, Lithuania) · 2022Review
- A comprehensive survey into the role of microRNAs in ovarian cancer chemoresistance; an updated overview.Journal of ovarian research · 2022Review
- miR-33a-5p inhibits the progression of esophageal cancer through the DKK1-mediated Wnt/β-catenin pathway.Aging · 2021Article
- MicroRNAs' role in the environment-related non-communicable diseases and link to multidrug resistance, regulation, or alteration.Environmental science and pollution research international · 2021Review
- Glutathione S-Transferase M3 Is Associated with Glycolysis in Intrinsic Temozolomide-Resistant Glioblastoma Multiforme Cells.International journal of molecular sciences · 2021Article
- Ferroptosis Holds Novel Promise in Treatment of Cancer Mediated by Non-coding RNAs.Frontiers in cell and developmental biology · 2021Review
- The Non-Coding RNAs Inducing Drug Resistance in Ovarian Cancer: A New Perspective for Understanding Drug Resistance.Frontiers in oncology · 2021Review
- Double Insurance for OC: miRNA-Mediated Platinum Resistance and Immune Escape.Frontiers in immunology · 2021Review
- The emerging roles of E3 ubiquitin ligases in ovarian cancer chemoresistance.Cancer drug resistance (Alhambra, Calif.) · 2021Review
- Mechanisms of Taxane ResistanceCancers · 2020Review
- Review
- Identification of the key genes associated with chemotherapy sensitivity in ovarian cancer patients.Cancer medicine · 2020Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAccumulating studies reveal that aberrant microRNA (miRNA) expression can affect the development of chemotherapy drug resistance by modulating the expression of relevant target proteins. The aim of this study was to investigate the role of miR-133b in the development of drug resistance in ovarian cancer cells.
methodsWe examined the levels of miR-133b expression in ovarian carcinoma tissues and the human ovarian carcinoma cell lines (A2780, A2780/DDP and A2780/Taxol, respectively). We determined the cell viability of these cell lines treated with cisplatin or paclitaxel in the presence or absence of miR-133b or anti-miR-133b transfection using the MTT assay. Reverse transcription polymerase chain reaction and Western blotting were used to assess the mRNA and protein expression levels of two drug-resistance-related genes: glutathione S-transferase (GST)-π and multidrug resistance protein 1 (MDR1). The dual-luciferase reporter assay was used to detect the promoter activity of GST-π in the presence and absence of miR-133b.
resultsThe expression of miR-133b was significantly lower in primary resistant ovarian carcinomas than in the chemotherapy-sensitive carcinomas (P<0.05), and the same results were found in primary resistant ovarian cell lines (A2780/Taxol and A2780/DDP) compared to the chemotherapy-sensitive cell line (A2780; P<0.05). Following miR-133b transfection, four cell lines showed increased sensitivity to paclitaxel and cisplatin, while anti-miR-133b transfection reduced cell sensitivity to paclitaxel and cisplatin. Dual-luciferase reporter assay showed that miR-133b interacted with the 3'-untranslated region of GST-π. Compared to controls, the mRNA and protein levels of MDR1 and GST-π were downregulated after miR-133b transfection and upregulated after anti-miR-133b transfection.
conclusionMicroRNA-133b may reduce ovarian cancer drug resistance by silencing the expression of the drug-resistance-related proteins, GST-π and MDR1. In future, the combination of miR-133b with chemotherapy agents may prevent the development of drug resistance in ovarian cancers.
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