ERα36, a variant of estrogen receptor α, is predominantly localized in mitochondria of human uterine smooth muscle and leiomyoma cells

Yan, Yuchao; Yu, Linda Chia‐Hui; Castro, Lysandra; Dixon, Darlene

doi:10.1371/journal.pone.0186078

Cited by 21 publications

(16 citation statements)

References 29 publications

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“…However, the ERα36 mRNA was also found in various healthy estrogen-sensitive tissues such as the mammary gland, the uterus, the bone and cartilage tissues, renal tubules, the stomach, etc. [31][32][33][34][35][36]. This suggested that this variant could participate in mediating the physiological effects of estrogens.…”

Section: Consequences Of Erα36 Expression In Non-cancerous Cellsmentioning

confidence: 96%

The Role of ERα36 in Development and Tumor Malignancy

Thiébaut

Konan

Guerquin

et al. 2020

IJMS

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Estrogen nuclear receptors, represented by the canonical forms ERα66 and ERβ1, are the main mediators of the estrogen-dependent pathophysiology in mammals. However, numerous isoforms have been identified, stimulating unconventional estrogen response pathways leading to complex cellular and tissue responses. The estrogen receptor variant, ERα36, was cloned in 2005 and is mainly described in the literature to be involved in the progression of mammary tumors and in the acquired resistance to anti-estrogen drugs, such as tamoxifen. In this review, we will first specify the place that ERα36 currently occupies within the diversity of nuclear and membrane estrogen receptors. We will then report recent data on the impact of ERα36 expression and/or activity in normal breast and testicular cells, but also in different types of tumors including mammary tumors, highlighting why ERα36 can now be considered as a marker of malignancy. Finally, we will explain how studying the regulation of ERα36 expression could provide new clues to counteract resistance to cancer treatments in hormone-sensitive tumors.

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Section: Consequences Of Erα36 Expression In Non-cancerous Cellsmentioning

confidence: 96%

The Role of ERα36 in Development and Tumor Malignancy

Thiébaut

Konan

Guerquin

et al. 2020

IJMS

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“…Fluorescence images were captured using a confocal laser-scanning microscope (Leica, Solms, Germany). The Image J Just Another Colocalization Plugin (JACoP) was applied for quantitative colocalization analyses [56].…”

Section: Immunofluorescence Stainingmentioning

confidence: 99%

A connexin43/YAP axis regulates astroglial-mesenchymal transition in hemoglobin induced astrocyte activation

et al. 2018

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Reactive astrogliosis is a common response to insults to the central nervous system, but the mechanism remains unknown. In this study, we found the temporal and spatial differential expression of glial fibrillary acidic protein (GFAP) and Vimentin in the intracerebral hemorrhage (ICH) mouse brain, indicating that the de-differentiation and astroglial-mesenchymal transition (AMT) of astrocytes might be an early event in reactive astrogliosis. Further we verified the AMT finding in purified astrocyte cultures exposed to hemoglobin (Hb). Additionally, Connexin 43 (Cx43) downregulation and YAP nuclear translocation were observed in Hb-activated astrocytes. Knocking down Cx43 by siRNA triggered YAP nuclear translocation. Cx43 and YAP were physically associated as determined by immunofluorescence and co-immunoprecipitation. We propose that astrocytes undergo AMT during Hb-induced activation where Cx43 downregulation facilitates YAP nuclear translocation is a novel mechanism involved in this process. Cx43-YAP interaction may represent a potential therapeutic target for modulating astrocyte activation.

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“…Estrogen controls various physiological and disease processes, especially reproduction, bone remodeling, and development of gynecologic cancer [2]. This increased occurrence of UEC has been attributed to the most common subtype of UEC, that is, type 1 estrogendependent UEC, which is comprised of grades 1 and 2 endometrioid adenocarcinoma [3,4].…”

Section: Introductionmentioning

confidence: 99%

“…This increased occurrence of UEC has been attributed to the most common subtype of UEC, that is, type 1 estrogendependent UEC, which is comprised of grades 1 and 2 endometrioid adenocarcinoma [3,4]. Estrogen receptors (ER) belong to the nuclear receptor superfamily, including estrogen receptor alpha (ERα), estrogen receptor beta (ERβ) and, estrogen-related receptors (ERRα, β, and γ) [2,5,6]. Estrogen triggers the proliferation, invasion and epithelial-mesenchymal transition (EMT) event of uterus endometrial cancer cells (UECC) and contributes to the pathogenesis and progression of UEC [7,8].…”

Section: Introductionmentioning

confidence: 99%

High Glucose Promotes Epithelial-Mesenchymal Transition of Uterus Endometrial Cancer Cells by Increasing ER/GLUT4-Mediated VEGF Secretion

Gu¹,

Xie²,

Zhang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Uterus endometrial cancer (UEC) is the common malignancy among gynecologic cancers, and most of them are type I estrogen-dependent UEC. Diabetes is well-known risk factor for the development of UEC. However, the underlying link between high glucose (HG) and the estrogen receptor in UEC remains unclear. Epithelial-mesenchymal transition (EMT) has also been shown to occur during the initiation of metastasis in cancer progression. The aim of this study was to determine the relationships and roles of HG, estrogen receptor and EMT in the growth and migration of UEC. Methods: The expression of glucose transport protein 4 (GLUT4) in the control endometrium and UEC tissues was detected by immunohistochemistry (IHC); the cell viability and invasion were analyzed through CCK-8 and Matrigel invasion assays; the transcriptional level of EMT-related genes was evaluated through real-time PCR; and the effect of HG and / or GLUT4 on estrogen receptors, vascular endothelial growth factor (VEGF) and its receptor VEGFR was analyzed through western blotting, ELISA and flow cytometry (FCM) assay, respectively. In addition, Ishikawa-xenografted nude mice were constructed and were used to analyze the effect of estrogen and GLUT4 on the growth of UEC in vivo. Results: Here, we found that exposure to HG led to a high level of viability and invasion of UEC cell lines (UECC, Ishikawa and RL95-2 cells). Compared with the normal endometrium, a higher level of GLUT4 was observed in UEC tissues. Silencing GLUT4 obviously inhibited the HG-promoted viability, invasion and expression of EMT-related genes (TWIST, SNAIL and CTNNB1) of UECC promoted by HG. Further analysis showed that HG and GLUT4 promoted the secretion of VEGF and expression of VEGFR in UECC. Treatment with HG led to the increase of estrogen receptor α (ERα) and β (ERβ) in UECC, blocking ERα or ERβ resulted in the decreases in GLUT4 expression, TWIST, SNAIL and CTNNB1 transcription, and VEGF and VEGFR expression in UECC. Treatment with anti-human VEGF neutralizing antibody restricted the viability and invasion of UECC that was induced by HG and estrogen. Exposure to estrogen accelerated growth, VEGF production, and TWIST and CTNNB1 expression in UEC in Ishikawa-xenografted nude mice, and silencing GLUT4 restricted these effects. Conclusion: These data suggest that HG increases GLUT4 and VEGF/VEGFR expression, further promotes EMT process and accelerates the development of UEC by up-regulating ER

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ERα36, a variant of estrogen receptor α, is predominantly localized in mitochondria of human uterine smooth muscle and leiomyoma cells

Cited by 21 publications

References 29 publications

The Role of ERα36 in Development and Tumor Malignancy

The Role of ERα36 in Development and Tumor Malignancy

A connexin43/YAP axis regulates astroglial-mesenchymal transition in hemoglobin induced astrocyte activation

High Glucose Promotes Epithelial-Mesenchymal Transition of Uterus Endometrial Cancer Cells by Increasing ER/GLUT4-Mediated VEGF Secretion

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