ArticleJournal of experimental & clinical cancer research : CR2018
ER-α36 mediates cisplatin resistance in breast cancer cells through EGFR/HER-2/ERK signaling pathway.
Article in Journal of experimental & clinical cancer research : CR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 30 citations in OpenAlex.
- Uncovering pan-cancer signatures of chemoresistance.Genome medicine · 2026Article
- Intelligent plant exosomes synergize miRNAs and cisplatin for spatiotemporally precise multimodal treatment for TNBC with high safety.Bioactive materials · 2026Article
- Nucleic sexual hormone receptor signaling pathways in breast cancer: function regulation, crosstalk, and therapeutic implications.NPJ precision oncology · 2026Review
- Regulatory network and spatial modeling reveal cooperative mechanisms of resistance and immune escape in ER+ breast cancer.BMC cancer · 2026Article
- Regulatory network and spatial modeling reveal cooperative mechanisms of resistance and immune escape in ER+ breast cancer.bioRxiv : the preprint server for biology · 2025Article
- TRPV1 inhibition overcomes cisplatin resistance by blocking autophagy-mediated hyperactivation of EGFR signaling pathway.Nature communications · 2023Article
- Research on the biological mechanism and potential application of CEMIP.Frontiers in immunology · 2023Review
- Estrogen alleviates post-traumatic osteoarthritis progression and decreases p-EGFR levels in female mouse cartilage.BMC musculoskeletal disorders · 2022Article
- Aldolase A promotes cell proliferation and cisplatin resistance via the EGFR pathway in gastric cancer.American journal of translational research · 2022Article
- Rewiring of the Endocrine Network in Triple-Negative Breast Cancer.Frontiers in oncology · 2022Review
- The Role of ERα36 in Development and Tumor Malignancy.International journal of molecular sciences · 2020Review
- Effects of cisplatin on the proliferation, invasion and apoptosis of breast cancer cells following β‑catenin silencing.International journal of molecular medicine · 2020Article
- Chlorotoxin targets ERα/VASP signaling pathway to combat breast cancer.Cancer medicine · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundER-α36, a novel ER-α66 variant, has been demonstrated to promote tamoxifen resistance in breast cancer cells. However, the role and mechanisms of ER-α36 in cisplatin resistance of breast cancer cells remain unclear. This study investigates the expression and role of ER-α36 in cisplatin resistance of breast cancer cells and elucidates its underlying mechanisms.
methodsThe expression of ER-α36 and the proteins involved in nongenomic estrogen signaling was evaluated by western blot analysis. Cisplatin sensitivity was explored by CCK-8 assay, monolayer colony formation assay and apoptosis assays, respectively. ER-α36 siRNAs/shRNAs and overexpression vector were transfected into cells to down-regulate or up-regulate ER-α36 expression. Loss-and gain-of function assays were performed to investigate the role of ER-α36 in cisplatin sensitivity. The interaction between ER-α36 and EGFR/HER-2 were detected using CoIP. A mouse xenograft model of breast cancer was established to verify the role of ER-α36 in vivo.
resultsER-α36 is expressed at higher levels in cisplatin-resistant breast cancer cells compared to cisplatin sensitive cells. Cisplatin induced up-regulation of ER-α36 in a dose-dependent manner in breast cancer cells. Overexpression of ER-α36 leaded to cell resistant to cisplatin and knockdown of ER-α36 in cisplatin-resistant breast cancer cells restored cisplatin sensitivity. The up-regulation of ER-α36 resulted in increased activation of nongenomic estrogen signaling, which was responsible for cisplatin resistance. Disruption of ER-α36-mediated nongenomic estrogen signaling with kinase inhibitors significantly inhibited cisplatin-induced expression of ER-α36 and increased cisplatin sensitivity. The in vivo experiment also confirmed that up-regulation of ER-α36 attenuated cisplatin sensitivity in a mouse xenograft model of breast cancer.
conclusionsThe results for the first time demonstrated that ER-α36 mediates cisplatin resistance in breast cancer cells through nongenomic estrogen signaling, suggesting that ER-α36 may serve as a novel target for cisplatin resistance and a potential indicator of cisplatin sensitivity in breast cancer treatment.
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