ArticleDiscover oncology2025
ESM1 suppresses LncRNA GAS5/miR-23a-3p/PTEN axis to promote the cisplatin-chemotherapy resistance of ovarian cancer cells via activating the PI3K/AKT pathway.
Article in Discover oncology, 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.
- Review
- ESM1 drives cancer angiogenesis and bevacizumab resistance via trioleate synthesis.Neoplasia (New York, N.Y.) · 2026Article
- ESM1 and protein lysine L-lactylation modification (Pan-kla) in ovarian cancer: coexpression, clinical significance, and prognostic value.Diagnostic pathology · 2026Article
- Long non-coding RNAs and VEGF in ovarian cancer: mechanisms and therapeutic potential.Journal of ovarian research · 2025Review
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14 authors.
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Abstract
backgroundCisplatin chemotherapy is an important treatment for advanced ovarian cancer (OC). However, the development of cisplatin resistance greatly limits the survival time of OC patients. Endothelial cell-specific molecule 1 (ESM1) has been found to be an important proto-oncogene promoting OC, but its mediating OC cisplatin resistance remains unknown.
methodsWe used quantitative polymerase chain reaction (qPCR) to measure transcription levels of ESM1, Growth arrest specific transcript 5 (GAS5), miR-23a-3p, and Phosphatase And Tensin Homolog (PTEN). A double luciferase reporter gene assay confirmed the direct binding of GAS5 to miR-23a-3p and miR-23a-3p to PTEN mRNA. The effects of ESM1, GAS5, miR-23a-3p, and PTEN on OC cisplatin resistance were tested with an Half Maximal Inhibitory Concentration (IC50) assay. Flow cytometry was used to assess the effects of ESM1, GAS5, and miR-23a-3p on cisplatin-induced OC apoptosis. Changes in apoptosis-related proteins and PI3K/AKT-related proteins were analyzed with western blot (WB).
resultsESM1 inhibits the levels of GAS5 and PTEN but increases miR-23a-3p. ESM1 and miR-23a-3p promote OC cisplatin resistance. GAS5 and miR-23a-3p promote cisplatin sensitivity for OC cells. Moreover, the main molecular mechanism is the ESM1/GAS5/miR-23a-3p/PTEN/PI3K/Akt signaling axis.
conclusionESM1 promotes OC cisplatin resistance by activating the Phosphoinositide-3-Kinase (PI3K)/AKT Serine/Threonine Kinase (Akt) signaling pathway through the GAS5/miR-23a-3p/PTEN signaling axis. This suggests that prescriptive ESM1 regulates key downstream molecular mechanisms via non-coding RNA and can be used before neoadjuvant chemotherapy in OC is initiated.
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