ArticleBMC women's health2024
Fanconi anemia complementation group D2 promotes sensitivity of endometrial cancer cells to chemotherapeutic agents by inhibiting the ferroptosis pathway.
Article in BMC women's health, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Ferroptosis as a novel targeted therapy in gynecological malignant tumors.Discover oncology · 2026Review
- Targeting FANCD2 to overcome enzalutamide resistance in prostate cancer.Cancer & metabolism · 2026Article
- Potential role of Fanconi anemia pathway in the pathogenesis of endometrial cancer (Review).Molecular medicine reports · 2025Review
- Mechanism of LncRNA NORAD regulating ferroptosis in endometrial cancer cells by modifying GPX4 through FTO-mediated m6A methylation.Cellular and molecular life sciences : CMLS · 2025Article
- The dual role of SLC7A11 in tumor drug resistance: mechanisms, challenges, and therapeutic potential.American journal of cancer research · 2025Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundResistance can develop during treatment of advanced endometrial cancer (EC), leading to unsatisfactory results. Fanconi anemia complementation group D2 (Fancd2) has been shown to be closely related to drug resistance in cancer cells. Therefore, this study was designed to explore the correlation of Fancd2 with EC resistance and the mechanism of Fancd2.
methodsReal-time quantitative PCR (RT-qPCR) was used to detect the expression of Fancd2 in EC tissues and cells. EC cells (Ishikawa) and paclitaxel-resistant EC cells (Ishikawa/TAX) were transfected to knock down Fancd2. In addition, the ferroptosis inhibitor Ferrostatin-1 was adopted to treat Ishikawa/TAX cells. The sensitivity of cancer cells to chemotherapeutic agents was observed via 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, and inhibitory concentration (IC)50 was calculated. Reactive oxygen species (ROS) levels were measured by flow cytometry, the activity of malondialdehyde (MDA) and the levels of glutathione (GSH) and Fe
resultsCompared with the normal tissues and endometrial epithelial cells, Fancd2 expression was significantly increased in EC tissues and Ishikawa cells, respectively. After knock-down of Fancd2, Ishikawa cells showed significantly increased sensitivity to chemotherapeutic agents. Besides, compared with Ishikawa cells, the levels of ROS, the activity of MDA, and the levels of GSH and Fe
conclusionFancd2 increases drug resistance in EC cells by inhibiting the cellular ferroptosis pathway.
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