ArticleScientific reports2025
Mechanistic insights into epithelial-mesenchymal transition mediated cisplatin resistance in ovarian cancer.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Exploring the chemical and biological interplay in phenanthroline-containing copper complexes.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Article
- Cisplatin-Resistant Lung Adenocarcinoma Cells Exhibit Increased Proangiogenic Capacity in a Microphysiological Model of Tumor Neovascularization.Cancer medicine · 2026Article
- Multiomics, pharmacogenomic, and structural characterization of NCCRP1 as a candidate therapeutic target in ovarian cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Systems-Level Mapping of the Tumor Microenvironment Reveals Immune-Mediated Mechanisms and Potential Targets in Platinum-Resistant Ovarian Cancer.Research square · 2026Article
- INHBA secreted by cancer-associated fibroblasts promotes cisplatin resistance and malignant progression of ovarian cancer via ENG-mediated suppression of apoptosis and induction of EMT.Journal of translational medicine · 2026Article
- Oncogenic EGFR Signaling as a Central Regulator of Chemoresistance in Ovarian Cancer: A Mechanistic Review.International journal of molecular sciences · 2026Review
- Systems-level analysis identifies IRF6 as an inhibitor of epithelial-mesenchymal transition.Journal of biological engineering · 2026Article
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Authors and funding
7 authors.
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Abstract
Epithelial-mesenchymal transition (EMT) is designated as one of the prime causes of chemoresistance in many cancers. In our previous study we established that cisplatin resistance in ovarian cancer (OC) is associated with EMT using sensitive OV90 cells and its resistant counterparts OV90CisR1 and OV90CisR2. In this study, we revealed through RNAseq analysis that ITGA1 can play essential part in EMT mediated cisplatin resistance in OC. We found large number of EMT related terms predominant in the top gene ontologies (GO). We also found Extracellular matrix (ECM) and actin cytoskeleton genes highly altered in the resistant cells. This was further confirmed by the protein-protein interaction (PPI) analysis where we identified that the core ECM components e.g., collagen, fibronectin, metalloproteases and integrins possessed most interactions. The pathway analysis revealed the Wnt signaling as the leading pathway. Since integrins have significant interaction with Wnt signaling, we focused our study on integrins among which, ITGA1, ITGA6, ITGA11 and ITGAV were primarily altered. We validated our results by western blotting and found that ITGA1 was highly expressed in resistant cells. Additionally, the high ABCA5 (efflux transporter) expression in resistant cells also supports the EMT proposition. The western blotting also revealed high β-catenin expression in resistant cells confirming the high Wnt signaling activity. Further, we induced xenograft tumors in nude mice. The histopathological analysis confirmed the aggressive nature of resistant tumors and showed the presence of necrotic core which could be implicated to EMT. Finally, the immunohistochemical staining confirmed the high protein expression in resistant tumor.
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