Expression of ERα36 in gastric cancer samples and their matched normal tissues

Wang, Jianjun; Li, Jiajia; Fang, Rengui; Xie, Shuduo; Wang, Linbo; Xu, Chaoyang

doi:10.3892/ol.2011.437

Cited by 13 publications

(8 citation statements)

References 20 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%

“…Although the expression of ERα36 is very high in several gastric cancer cell lines (SGC-7901, AGS, BGC-923, and MKN-45), two independent clinical studies regarding the expression of ERα36 in gastric cancer produced conflicting results. Indeed, in these two studies, the amount of ERα36 mRNA in cancer samples is alternately higher [72] or lower [33] than in normal tissue and ERα36 expression was not significantly associated with gender, age, grading, size of the tumor, or lymph node metastasis. However, ERα-36 expression positively correlated with Cyclin D1 and GRP94, two downstream effectors of ERα36-mediated non genomic estrogen signaling that could help to explain ERα36 function during gastric carcinogenesis [72,73].…”

Section: Gastric Cancermentioning

confidence: 99%

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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%

Section: Gastric Cancermentioning

confidence: 99%

The Role of ERα36 in Development and Tumor Malignancy

Thiébaut

Konan

Guerquin

et al. 2020

IJMS

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“…This is also supported by our evidence that the estrogen receptor variant ERα36 was detected specifically in the female LGKO with liver tumors. Fourth, although it is not currently clear about how ERα36 mechanistically causes or regulates hepatic tumorigenesis, overexpression of ERα36 has been linked to carcinogenesis in other systems such as breast cancer and gastric cancer . Therefore, by combining the information from the literature with our results, we propose a specific link of long‐term ER stress with HCA in females.…”

Section: Discussionmentioning

confidence: 65%

Association of cyclin D and estrogen receptor α36 with hepatocellular adenomas of female mice under chronic endoplasmic reticulum stress

Lau

Han

et al. 2013

J of Gastro and Hepatol

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Background & Aims Hepatocellular adenomas (HCA) are benign tumors that can lead to medical complications. Chronic inflammation and mutations in β-catenin, HNF1α or GP130 are potential causes for human HCA. However, additional causes may exist due to heterogeneity of HCA. We investigated whether HCA are caused by endoplasmic reticulum (ER) stress. Methods Mice with a liver specific deletion of the major chaperone BiP (LGKO) were used. Liver tumor occurrence was examined in LGKO with or without feeding of a high fat diet (HFD) and characterized with immunohistochemistry with molecular markers of proliferation/malignancy. Molecular changes were analyzed with immunoblotting. Results Spontaneous monoclonal liver tumors were observed in 34% of LGKO females with constitutive hepatic ER stress. Lack of portal tracks or central veins, dilated sinusoidal spaces, hemorrhagic areas, active proliferation and Lipid deposits were observed in the liver tumors. HFD feeding induced multi-clonal liver tumors in 83% of the LGKO females versus zero in wild type females. Hepatocytes reactive to anti-glypican-3 antibodies were detected in the HFD-induced but not spontaneous tumors. In the liver tumors, inhibition of cyclin D and increase of the 36kD estrogen receptor variant (ERα36), active ATF4/6, GSK3β and ERK1/2 were detected whereas no change of HNF1α, β-catenin, p-53, androgen receptor α or estrogen receptor α was detected. HFD activated JAK and STAT3. Conclusions Our evidence supports a possible link of HCA with ER stress and altered expression of cyclin D and ERα36. Additional stress such as HFD may promote malignant transformation of HCA through the JAK-STAT pathway.

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“…Overexpression of coactivators, for example coactivator-associated arginine methyltransferase 1, may also increase the expression of ERα target genes involved in breast tumor cell differentiation and proliferation ( 26 ), including breast cancer (BRCA) 1 and BRCA2 genes ( 27 ). In addition, reduction of ERα spliced variant 46 (46 kDa) and 36 (36 kDa) mRNA levels have been observed in colon tumors ( 28 ) and overexpression of ERα36 has been observed in gastric ( 29 ) and endometrial cancers ( 30 ).…”

Section: Er Proteins and Tumor Diseasesmentioning

confidence: 99%

Identification of estrogen receptor proteins in breast cancer cells using matrix-assisted laser desorption/ionization time of flight mass spectrometry (Review)

et al. 2014

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Estrogen receptors [ERs (subtypes α and β)], classified as a nuclear receptor super family, are intracellular proteins with an important biological role as the transcription factors for estrogen target genes. For ER-induced transcription, an interaction must exist between ligand and coregulators. Coregulators may stimulate (coactivators) or inhibit (corepressors) transcription, following binding with a specific region of the gene, called the estrogen response element. Misbalanced activity of coregulators or higher ligand concentrations may cause increased cell proliferation, resulting in specific types of cancer. These are exhibited as overexpression of ER proteins. Breast cancer currently ranks first in the incidence and second in the mortality of cancer in females worldwide. In addition, 70% of breast tumors are ERα positive and the importance of these proteins for diagnostic use is indisputable. Early diagnosis of the tumor and its classification has a large influence on the selection of appropriate therapy, as ER-positive tumors demonstrate a positive response to hormonal therapy. Matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI TOF MS) has been hypothesized to have great potential, as it offers reliable, robust and efficient analysis methods for biomarker monitoring and identification. The present review discusses ER protein analysis by MALDI TOF MS, including the crucial step of protein separation.

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Expression of ERα36 in gastric cancer samples and their matched normal tissues

Cited by 13 publications

References 20 publications

The Role of ERα36 in Development and Tumor Malignancy

The Role of ERα36 in Development and Tumor Malignancy

Association of cyclin D and estrogen receptor α36 with hepatocellular adenomas of female mice under chronic endoplasmic reticulum stress

Identification of estrogen receptor proteins in breast cancer cells using matrix-assisted laser desorption/ionization time of flight mass spectrometry (Review)

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