Estrogen receptor-α36 is involved in development of acquired tamoxifen resistance via regulating the growth status switch in breast cancer cells. - Wikidata - awgldk - TriplyDB

Estrogen receptor-α36 is involved in development of acquired tamoxifen resistance via regulating the growth status switch in breast cancer cells.

Estrogen receptor-α36 is involved in development of acquired tamoxifen resistance via regulating the growth status switch in breast cancer cells.

http://www.wikidata.org/entity/Q41134570

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Roles for miRNAs in endocrine resistance in breast cancer The therapeutic target of estrogen receptor-alpha36 in estrogen-dependent tumors Estrogen receptor-α36 is involved in pterostilbene-induced apoptosis and anti-proliferation in in vitro and in vivo breast cancer ER-α36: a novel biomarker and potential therapeutic target in breast cancer.Disruption of the ER-α36-EGFR/HER2 positive regulatory loops restores tamoxifen sensitivity in tamoxifen resistance breast cancer cells Luteolin exerts a marked antitumor effect in cMet-overexpressing patient-derived tumor xenograft models of gastric cancer MicroRNA-125b upregulation confers aromatase inhibitor resistance and is a novel marker of poor prognosis in breast cancer From ERα66 to ERα36: a generic method for validating a prognosis marker of breast tumor progression.Chaperone gp96 mediates ER-α36 cell membrane expression.Multidrug-resistant breast cancer: current perspectives.Role of ER-α36 in breast cancer by typical xenoestrogens.Tamoxifen resistance and metastasis of human breast cancer cells were mediated by the membrane-associated estrogen receptor ER-α36 signaling in vitro.Lower Beclin 1 downregulates HER2 expression to enhance tamoxifen sensitivity and predicts a favorable outcome for ER positive breast cancer Concomitant high expression of ERα36, EGFR and HER2 is associated with aggressive behaviors of papillary thyroid carcinomas.ERα36, a variant of estrogen receptor α, is predominantly localized in mitochondria of human uterine smooth muscle and leiomyoma cells.Extranuclear signaling by sex steroid receptors and clinical implications in breast cancer.Identification of a novel human estrogen receptor-α splice variant able to enhance malignant biological behaviors of breast cancer cells.Structural insights into tumor-specific chaperoning activity of gamma synuclein in protecting estrogen receptor alpha 36 and its role in tamoxifen resistance in breast cancer.Endocrine Resistance in Breast Cancer

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Estrogen receptor-α36 is involved in development of acquired tamoxifen resistance via regulating the growth status switch in breast cancer cells.

http://www.wikidata.org/entity/Q41134570

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J.MOLONC.2013.02.001

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Molecular Oncology

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Estrogen receptor-α36 is invol ...... switch in breast cancer cells.

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Guangliang Li

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Haiyong Wang

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Haohao Wang

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Jiang Cao

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Jing Zhang

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Ketao Jin

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Kuifeng He

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Lisong Teng

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Xiaodong Teng

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Xin Xu

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P2860

A positive feedback loop of ER-α36/EGFR promotes malignant growth of ER-negative breast cancer cells

Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method

Cancer statistics, 2011: the impact of eliminating socioeconomic and racial disparities on premature cancer deaths

A synthetic inhibitor of the mitogen-activated protein kinase cascade

PD 098059 is a specific inhibitor of the activation of mitogen-activated protein kinase kinase in vitro and in vivo

Signal transducer and activator of transcription 5b, c-Src, and epidermal growth factor receptor signaling play integral roles in estrogen-stimulated proliferation of estrogen receptor-positive breast cancer cells.

Long-term treatment with tamoxifen facilitates translocation of estrogen receptor alpha out of the nucleus and enhances its interaction with EGFR in MCF-7 breast cancer cells.

Estrogen signals via an extra-nuclear pathway involving IGF-1R and EGFR in tamoxifen-sensitive and -resistant breast cancer cells.

ER-alpha36, a variant of ER-alpha, promotes tamoxifen agonist action in endometrial cancer cells via the MAPK/ERK and PI3K/Akt pathways.

ER-α36, a novel variant of ER-α, mediates estrogen-stimulated proliferation of endometrial carcinoma cells via the PKCδ/ERK pathway.

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10.1016/J.MOLONC.2013.02.001

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