Cytoplasm estrogen receptor β5 as an improved prognostic factor in thymoma and thymic carcinoma progression

Li, Sheng-Ying; Wang, Yuxia; Wang, Lei; Qian, Zhi‐Bing; Ji, Mingli

doi:10.3892/ol.2015.3555

Cited by 3 publications

(3 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our studies in endometrial cancer tissue are in agreement with other results reporting expression of ERβ5 protein is upregulated in a number of hormone-responsive cancers compared with equivalent non-malignant tissues (Li et al . 2015).…”

Section: Discussionsupporting

confidence: 93%

See 1 more Smart Citation

The ERβ5 splice variant increases oestrogen responsiveness of ERαpos Ishikawa cells

Collins

Itani

Esnal-Zufiaurre

et al. 2020

Endocrine-Related Cancer

View full text Add to dashboard Cite

Endometrial cancer is a common gynaeological malignancy: life time exposure to oestrogen is a key risk factor. Oestrogen action is mediated by receptors encoded by ESR1 (ERα) and ESR2 (ERβ): ERα plays a key role in regulating endometrial cell proliferation. A truncated splice variant isoform (ERβ5) encoded by ESR2 is highly expressed in cancers. This study explored whether ERβ5 alters oestrogen responsiveness of endometrial epithelial cells. Immunhistochemistry profiling of human endometrial cancer tissue biopsies identified epithelial cells co-expressing ERβ5 and ERα in stage I endometrial adenocarcinomas and post menopausal endometrium. Induced co-expression of ERβ5 in ERαpos endometrial cancer cells (Ishikawa) significantly increased ligand-dependent activation of an ERE-luciferase reporter stimulated by either E2 or the ERα-selective agonist 1,3,5-(4-hydroxyphenyl)-4-propyl-1H-pyrazole (PPT) compared to untransfected cells. Fluorescence recovery after photobleaching (FRAP) analysis of tagged yellow fluorescent protein (YFP)-ERβ5 transfected into Ishikawa cells revealed that incubation with E2 induced a transient reduction in intra-nuclear mobility characterised by punctate protein redistribution which phenocopied the behaviour of ERα following ligand activation with E2. In ERαneg MDA-MD-231 breast cancer cells, there was no E2-dependent change in mobility of YFP-ERβ5 and no activation of the ERE reporter in cells expressing ERβ5. In conclusion, we demonstrate that ERβ5 can act as heterodimeric partner to ERα in Ishikawa cells and increases their sensitivity to E2. We speculate that expression of ERβ5 in endometrial epithelial cells may increase the risk of malignant transformation and suggest that immunostaining for ERβ5 should be included in diagnostic assessment of women with early grade cancers.

show abstract

Section: Discussionsupporting

confidence: 93%

“…Over-expression of ERβ5 has also been reported in colon cancers (Wong et al . 2005), glioma (Li et al 2013), cancers of the ovary (Ciucci et al 2014) and of the thymus (Li et al 2015); however, to date, the impact of ERβ5 in endometrial cancers is unknown.…”

Section: Introductionmentioning

confidence: 99%

The ERβ5 splice variant increases oestrogen responsiveness of ERαpos Ishikawa cells

Collins

Itani

Esnal-Zufiaurre

et al. 2020

Endocrine-Related Cancer

View full text Add to dashboard Cite

show abstract

“…Finally, in a study published in 2015 the expression levels of the ERβ5 variant were analyzed in a set of tissue microarrays from a cohort of patients with thymic tumors (n=103) by immunohistochemistry (98). The results revealed that ERβ5 was overexpressed and predominantly located in the cytoplasm (cERβ5) of thymic tumors.…”

Section: Subtypes: Thymoma Thymic Carcinomamentioning

confidence: 99%

Expression and clinical implications of estrogen receptors in thoracic malignancies: a narrative review

Pinton¹,

Manzotti²,

Balzano³

et al. 2021

J Thorac Dis

View full text Add to dashboard Cite

Thoracic malignancies represent a significant global health burden with incidence and mortality increasing year by year. Thoracic cancer prognosis and treatment options depend on several factors, including the type and size of the tumor, its location, and the overall health status of patients. Gender represents an important prognostic variable in thoracic malignancies. One of the greatest biological differences between women and men is the presence of female sex hormones, and an increasing number of studies suggest that estrogens may play either a causative or a protective role in thoracic malignancies. Over the past 60 years since the discovery of the first nuclear estrogen receptor (ER) isoform α and the almost 20 years since the discovery of the second estrogen receptor, ERβ, different mechanisms governing estrogen action have been identified and characterized. This literature review reports the published data regarding the expression and function of ERs in different thoracic malignancies and discuss sex disparity in clinical outcomes. From this analysis emerges that further efforts are warranted to better elucidate the role of sex hormones in thoracic malignancies, and to reduce disparities in care between genders. Understanding the mechanisms by which gender-related differences can affect and interfere with the onset and evolution of thoracic malignancies and impact on response to therapies could help to improve the knowledge needed to develop increasingly personalized and targeted treatments.

show abstract

Genes Co-Expressed with ESR2 Influence Clinical Outcomes in Cancer Patients: TCGA Data Analysis

Lipowicz,

Malińska,

Nowicki

et al. 2024

IJMS

View full text Add to dashboard Cite

ERβ has been assigned a tumor suppressor role in many cancer types. However, as conflicting findings emerge, ERβ’s tissue-specific expression and functional role have remained elusive. There remains a notable gap in compact and comprehensive analyses of ESR2 mRNA expression levels across diverse tumor types coupled with an exploration of its potential gene network. In this study, we aim to address these gaps by presenting a comprehensive analysis of ESR2 transcriptomic data. We distinguished cancer types with significant changes in ESR2 expression levels compared to corresponding healthy tissue and concluded that ESR2 influences patient survival. Gene Set Enrichment Analysis (GSEA) distinguished molecular pathways affected by ESR2, including oxidative phosphorylation and epithelial–mesenchymal transition. Finally, we investigated genes displaying similar expression patterns as ESR2 in tumor tissues, identifying potential co-expressed genes that may exert a synergistic effect on clinical outcomes, with significant results, including the expression of ACIN1, SYNE2, TNFRSF13C, and MDM4. Collectively, our results highlight the significant influence of ESR2 mRNA expression on the transcriptomic landscape and the overall metabolism of cancerous cells across various tumor types.

show abstract

Cytoplasm estrogen receptor β5 as an improved prognostic factor in thymoma and thymic carcinoma progression

Cited by 3 publications

References 30 publications

The ERβ5 splice variant increases oestrogen responsiveness of ERαpos Ishikawa cells

The ERβ5 splice variant increases oestrogen responsiveness of ERαpos Ishikawa cells

Expression and clinical implications of estrogen receptors in thoracic malignancies: a narrative review

Genes Co-Expressed with ESR2 Influence Clinical Outcomes in Cancer Patients: TCGA Data Analysis

Contact Info

Product

Resources

About