ArticleCancer science2019
Estrogen receptor variant ER-α36 promotes tamoxifen agonist activity in glioblastoma cells.
Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 36 citations in OpenAlex.
- Targeting caveolin-1: dual challenges in tumor immunity and drug therapy strategies.Cancer cell international · 2026Review
- Evaluation of (Z)-endoxifen as a potential therapy for glioblastoma multiforme through computational and experimental analyses.Scientific reports · 2025Article
- ER‑α36 knockdown is associated with lysosomal dysfunction and proliferation inhibition in liver cancer cells.Molecular medicine reports · 2025Article
- Neuropeptide Signaling in Glioblastoma: A Comprehensive Review of the Current State and Future Direction.Neuromolecular medicine · 2025Review
- Estrogen α and β Receptor Expression in the Various Regions of Resected Glioblastoma Multiforme Tumors and in an In Vitro Model.International journal of molecular sciences · 2024Article
- Localisation of oestrogen receptors in stem cells and in stem cell-derived neurons of the mouse.Journal of neuroendocrinology · 2023Article
- Targeting Options of Tumor-Associated Macrophages (TAM) Activity in Gliomas.Current neuropharmacology · 2023Review
- Review
- Review
- Integrative analysis of transcriptome complexity in pig granulosa cells by long-read isoform sequencing.PeerJ · 2022Article
- Hormone exposure and its suppressive effect on risk of high-grade gliomas among patients with breast cancer.Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia · 2021Article
- Estrogen Receptors as Molecular Targets of Endocrine Therapy for Glioblastoma.International journal of molecular sciences · 2021Review
- Astrocytoma: A Hormone-Sensitive Tumor?International journal of molecular sciences · 2020Review
- Study of immune responses in mice to oral administration of Flor·Essence.Molecular and clinical oncology · 2020Article
- Glioblastoma chemoresistance: roles of the mitochondrial melatonergic pathway.Cancer drug resistance (Alhambra, Calif.) · 2020Review
- A Role for Estrogen Receptor alpha36 in Cancer Progression.Frontiers in endocrinology · 2020Review
- Evaluation of Cytotoxic Effect of Cholesterol End-Capped Poly(International journal of nanomedicine · 2020Article
- Estrogen receptor variant ER-α36 promotes tamoxifen agonist activity in glioblastoma cells.Cancer science · 2019Article
- Nuclear and membrane-bound hormone receptors in glioblastoma: Expression, functionality, and therapeutic implications.Neuro-oncology advancesReview
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Glioblastoma (GBM) is a highly infiltrative and malignant primary brain tumor. Despite aggressive therapy, patients with GBM have a dismal prognosis with median survival of approximately 1 year. Tamoxifen (TAM), a selective estrogen receptor modulator (SERM), has been used to treat GBM for many years. ER-α36 is a novel variant of estrogen receptor-alpha66 (ER-α66) and can mediate cell proliferation through estrogen or anti-estrogen signaling in different cancer cells. Previously, we found that ER-α36 was highly expressed in GBM and was involved in the tamoxifen sensitivity of glioblastoma cells. However, the molecular mechanism responsible has not been well established. Here, we found that ER-α36 is highly expressed in glioblastoma specimens. We further found that ER-α36 knockdown increased sensitivity of glioblastoma U87 cells to TAM and decreased autophagy in these cells. However, ER-α36 overexpression decreased TAM sensitivity and induced autophagy. We also established TAM-resistant glioblastoma U251 cells by a long-term culture in TAM-containing medium and found that TAM-resistant cells showed a six-fold increase of ER-α36 mRNA expression and elevated basal autophagy. ER-α36 knockdown in these TAM-resistant cells restored TAM sensitivity. In addition, we recapitulated the physiologically relevant tumor microenvironment in an integrated microfluidic device, and U87 cells were treated with a gradient of TAM. We found that ER-α36 expression is consistent with autophagy protein P62 in a three-dimensional microenvironment. In summary, these results indicate that ER-α36 contributes to tamoxifen resistance in glioblastoma cells presumably through regulation of autophagy.
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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 OpenQuestion graph.