The therapeutic target of estrogen receptor-alpha36 in estrogen-dependent tumors

Gu, Yu; Chen, Tianxiang; López, Elena; Wu, Weizhu; Wang, Xiangdong; Cao, Jiashu; Teng, Lisong

doi:10.1186/1479-5876-12-16

Cited by 28 publications

(26 citation statements)

References 77 publications

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“…The fact that wtERa is reduced in HCC and wtERa functions as a tumor suppressor may well explained the failure of early trial of tamoxifen, as wtER antagonist, to treat HCC [6, 28]. However, recent studies have indicated that tamoxifen may inhibit HCC via ER-independent mechanisms [29]. …”

Section: Discussionmentioning

confidence: 99%

“…ERa36 may facilitate the growth, invasion and metastasis of cancers via various pathways including cancer stem/progenitor cells, and AKT survival signaling [28]. It is thus reasonable to consider it as a potential therapeutic target [29]. The finding of the increased ERa36 in HCC may suggest that HCC patients may also benefit from targeting ERa36.…”

Section: Discussionmentioning

confidence: 99%

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Alternative splicing of estrogen receptor alpha in hepatocellular carcinoma

et al. 2016

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BackgroundThe role of estrogen receptor alpha (ERa), estrogen receptor beta (ERb) and ERa36 signaling in hepatocellular carcinoma (HCC) is not fully addressed.MethodsIn this study, three cohorts were included: (i) primary HCC patients (N = 76, cohort P), (ii) colorectal liver metastasis (mCRC) (N = 32, cohort S), and (iii) HCC from The Cancer Genome Atlas (TCGA) (N = 121). The levels of ERa36 and wtER36 were measured and their correlation with clinicopathologic features was determined.ResultsWtERa was downregulated and that ERa36 was upregulated in tumor tissues in both cohort P and TCGA data set. ERa36 was downregulated in tumor tissues in cohort S. In cohort P, wtERa was differentially expressed in gender (P < 0.000), age (P = 0.004), tumor number (P = 0.043), tumor size (P = 0.002), intrahepatic recurrence (P = 0.054). ERa36 was unequally expressed in different non-tumor liver status (P = 0.040). WtERa was negatively associated with overall survival (OS) and disease free survival (DFS) in cohort P. Compared with non-tumor tissues, the expression of ERa36 was increased in primary HCC but decreased in secondary HCC, showing opposite expression patterns of ERa36 between primary HCC and secondary HCC.ConclusionsPrimary HCC is associated with the decreased WtERa but increased ERa36. The expression pattern of ERa36 is different between primary HCC and secondary HCC, as the former with the increased ERa36 but the latter with the decreased ERa36. Therefore, the expression of ERa36 may be used to differentiate the primary HCC and the secondary one.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Alternative splicing of estrogen receptor alpha in hepatocellular carcinoma

et al. 2016

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“…Non-genomically, estrogen may support breast tumor growth through ER-like proteins in the membrane. This is now under investigation [93].…”

Section: Discussionmentioning

confidence: 92%

Integrin αvβ3 in the Mediating Effects of Dihydrotestosterone and Resveratrol on Breast Cancer Cell Proliferation

Shih

et al. 2020

IJMS

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Hormones and their receptors play an important role in the development and progression of breast cancer. Hormones regulate the proliferation of breast cancer cells through binding between estrogen or progestins and steroid receptors that may reside in the cytoplasm or be transcriptionally activated as steroid-protein nuclear receptor complexes. However, receptors for nonpeptide hormones also exist in the plasma membrane. Via those receptors, hormones are able to stimulate breast cancer cell proliferation when activated. Integrins are heterodimeric structural proteins of the plasma membrane. Their primary functions are to interact with extracellular matrix proteins and growth factors. Recently, integrin αvβ3 has been identified as a receptor for nonpeptide hormones, such as thyroid hormone and dihydrotestosterone (DHT). DHT promotes the proliferation of human breast cancer cells through binding to integrin αvβ3. A receptor for resveratrol, a polyphenol stilbene, also exists on this integrin in breast cancer cells, mediating the anti-proliferative, pro-apoptotic action of the compound in these cells. Unrelated activities of DHT and resveratrol that originate at integrin depend upon downstream stimulation of mitogen-activated protein kinase (MAPK, ERK1/2) activity, suggesting the existence of distinct, function-specific pools of ERK1/2 within the cell. This review will discuss the features of these receptors in breast cancer cells, in turn suggesting clinical applications that are based on the interactions of resveratrol/DHT with integrin αvβ3 and other androgen receptors.

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“…They mediate the impacts of the estrogen hormone (Zhang et al, 2014). Estrogen regulates growth, homeostasis and differentiation in eukaryotic cells but it can increase the risk of breast and endometrial cancer too (Gu et al, 2014). Mitogenic functions of estrogen in etiology of breast cancer is well-documented (Duong et al, 2006).…”

Section: Estrogen Receptor Beta (Erβ) May Act As Mediator In Apoptotimentioning

confidence: 99%

Estrogen Receptor Beta (ERβ) May Act as Mediator in Apoptotic Induction of Grape Seed Extract (GSE)

Abroodi

Sajedi

Nikbakht

et al. 2019

Asian Pac J Cancer Prev

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Background: Grape seed extract is a complex mixture of polyphenols. Its anti-tumor effects have been reported by several studies. Estrogen receptors (ERs) are commonly considered as important markers for breast cancer. The present study aimed to evaluate the apoptotic effects of GSE on MCF7 breast cancer cells and assessed the expression of ERβ during treatment of cells with GSE. Material and Methods: The half maximal inhibitory concentration (IC 50 ) of GSE in MCF7 breast cancer cells were calculated by treating cells with serial dilution of GSE for 48 hours and cell viability evaluated using MTT assay. Then cells assigned to three groups: control (no treatment), DMSO (cells treated with 0.05% of DMSO) and GSE group (cells treated with of GSE for 48 hours). The apoptosis assay was performed by detecting Annexin V protein by flow cytometry. The gene expression of ERβ and caspase-3 was evaluated by Real-Time PCR. Results: Cells in GSE group treated with GSE IC 50 concentration for 48 hours. Annexin V staining assay, represented early apoptosis detected by flow cytometry analysis showed significantly higher expression (p<0.01) than control and DMSO groups. Moreover, results of Real-Time PCR showed a significant expression in ERβ and caspase-3 genes in GSE group compared to control and DMSO groups (Fold change = 2.3 and 3.5, respectively). Conclusion: GSE may induce apoptosis in MCF7 human breast cancer cells by activation of ERβ gene.

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The therapeutic target of estrogen receptor-alpha36 in estrogen-dependent tumors

Cited by 28 publications

References 77 publications

Alternative splicing of estrogen receptor alpha in hepatocellular carcinoma

Alternative splicing of estrogen receptor alpha in hepatocellular carcinoma

Integrin αvβ3 in the Mediating Effects of Dihydrotestosterone and Resveratrol on Breast Cancer Cell Proliferation

Estrogen Receptor Beta (ERβ) May Act as Mediator in Apoptotic Induction of Grape Seed Extract (GSE)

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