ArticlePloS one2010
ER-α36, a novel variant of ER-α, mediates estrogen-stimulated proliferation of endometrial carcinoma cells via the PKCδ/ERK pathway.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 65 citations in OpenAlex.
- When Estrogen Signaling Refuses to Die: Receptor Rewiring, Compartmentalization, and Endocrine Plasticity in Gynecological Cancers.International journal of molecular sciences · 2026Review
- ERα36 PromotesInternational journal of molecular sciences · 2025Article
- Review
- ER-α36 is involved in calycosin inhibition of IL-6 production in macrophages.Journal of cellular and molecular medicine · 2024Article
- Single-cell analysis of gastric signet ring cell carcinoma reveals cytological and immune microenvironment features.Nature communications · 2023Article
- The Co-Expression of Estrogen Receptors ERα, ERβ, and GPER in Endometrial Cancer.International journal of molecular sciences · 2023Article
- The E3 Ligase TRIM4 Facilitates SET Ubiquitin-Mediated Degradation to Enhance ER-α Action in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Estrogen Receptors-Mediated Apoptosis in Hormone-Dependent Cancers.International journal of molecular sciences · 2022Review
- [Estradiol activates ERK phosphorylation by binding to ERβ to inhibit proliferation and promote apoptosis of human chondrocytes].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- ER-α36 Promotes the Malignant Progression of Cervical Cancer Mediated by EstrogenFrontiers in oncology · 2021Article
- The miR-30a-5p/CLCF1 axis regulates sorafenib resistance and aerobic glycolysis in hepatocellular carcinoma.Cell death & disease · 2020Article
- ERα-36 regulates progesterone receptor activity in breast cancer.Breast cancer research : BCR · 2020Article
- Distribution and Prognostic Significance of Estrogen ReceptorJournal of thyroid research · 2020Article
- Progress in the Understanding of the Mechanism of Tamoxifen Resistance in Breast Cancer.Frontiers in pharmacology · 2020Review
- A Role for Estrogen Receptor alpha36 in Cancer Progression.Frontiers in endocrinology · 2020Review
- A nongenomic mechanism for "metalloestrogenic" effects of cadmium in human uterine leiomyoma cells through G protein-coupled estrogen receptor.Archives of toxicology · 2019Article
- Trastuzumab induces PUMA-dependent apoptosis and inhibits tumor growth in gastric cancer.FEBS open bio · 2018Article
- Sphingosine kinase 1 activation by estrogen receptor α36 contributes to tamoxifen resistance in breast cancer.Journal of lipid research · 2018Article
- BKCa participates in E2 inducing endometrial adenocarcinoma by activating MEK/ERK pathway.BMC cancer · 2018Article
- Phytonutrient genistein is a survival factor for pancreatic β-cells via GPR30-mediated mechanism.The Journal of nutritional biochemistry · 2018Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundRecently, a variant of ER-α, ER-α36 was identified and cloned. ER-α36 lacks intrinsic transcription activity and mainly mediates non-genomic estrogen signaling. The purpose of this study was to investigate the function and the underlying mechanisms of ER-α36 in growth regulation of endometrial Ishikawa cancer cells.
methodsThe cellular localization of ER-α36 and ER-α66 were determined by immunofluorescence in the Ishikawa cells. Ishikawa endometrial cancer control cells transfected with an empty expression vector, Ishikawa cells with shRNA knockdown of ER-α36 (Ishikawa/RNAiER36) and Ishikawa cells with shRNA knockdown of ER-α66 (Ishikawa/RNAiER66) were treated with E2 and E2-conjugated to bovine serum albumin (E2-BSA, membrane impermeable) in the absence and presence of different kinase inhibitors HBDDE, bisindolylmaleimide, rottlerin, H89 and U0126. The phosphorylation levels of signaling molecules and cyclin D1/cdk4 expression were examined with Western blot analysis and cell growth was monitored with the MTT assay.
resultsImmunofluorescence staining of Ishikawa cells demonstrated that ER-α36 was expressed mainly on the plasma membrane and in the cytoplasm, while ER-α66 was predominantly localized in the cell nucleus. Both E2 and E2-BSA rapidly activated PKCδ not PKCα in Ishikawa cells, which could be abrogated by ER-α36 shRNA expression. E2-and E2-BSA-induced ERK phosphorylation required ER-α36 and PKCδ. However, only E2 was able to induce Camp-dependent protein kinase A (PKA) phosphorylation. Furthermore, E2 enhances cyclin D1/cdk4 expression via ER-α36.
conclusionE2 activates the PKCδ/ERK pathway and enhances cyclin D1/cdk4 expression via the membrane-initiated signaling pathways mediated by ER-α36, suggesting a possible involvement of ER-α36 in E2-dependent growth-promoting effects in endometrial cancer cells.
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