ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
FOXA1-mediated transcription of MFAP2 facilitates cell growth, metastasis and cisplatin resistance in uterine corpus endometrial carcinoma.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Differential Effects of Mesenchymal Stem Cell- and Natural Killer Cell-Derived Extracellular Vesicles on Cisplatin Responsiveness in Endometrial Cancer Cells.International journal of molecular sciences · 2026Article
- ALKBH5 promotes the progression of cisplatin-resistant oral squamous cell carcinoma by regulating FOXA1 expression via mDaru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Article
- SETD7-mediated epigenetic regulation of LncRNA XIST promotes trophoblast pyroptosis: a study in preeclampsia mouse and cell models.Biology direct · 2026Article
- Article
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Authors and funding
3 authors.
Funding
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Abstract
Microfibril-associated protein 2 (MFAP2) has been confirmed to be an oncogene to participate in regulating the progression of many cancers. However, its role and mechanism in the development of uterine corpus endometrial carcinoma (UCEC) are still unclear. The mRNA and protein levels of MFAP2 and forkhead box A1 (FOXA1) were determined using qRT-PCR and western blot. Cell proliferation, apoptosis, migration, invasion and cisplatin resistance were detected by colony formation assay, EdU assay, flow cytometry, transwell assay and CCK8 assay. Xenograft tumor models were constructed to explore the effect of MFAP2 knockdown on UCEC tumorigenesis and cisplatin resistance in vivo. The interaction between FOXA1 and MFAP2 promoter was evaluated by ChIP assay and dual-luciferase reporter assay. MFAP2 was upregulated in UCEC tissues and cells. Silencing of MFAP2 repressed UCEC cell growth, metastasis and cisplatin resistance in vitro, as well as reduced tumorigenesis in vivo. In terms of mechanism, FOXA1 bound to MFAP2 promoter region to increase its expression. FOXA1 knockdown could inhibit UCEC cell growth, metastasis and cisplatin resistance. Moreover, FOXA1 promoted growth, metastasis and cisplatin resistance in UCEC cells via enhancing MFAP2 expression. FOXA1-activated MFAP2 might contribute to the growth, metastasis and cisplatin resistance of UCEC cells, providing a novel target for UCEC treatment.
Indexed as
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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 Socratic graph.