TOX3 is expressed in mammary ER+ epithelial cells and regulates ER target genes in luminal breast cancer

Seksenyan, Akop; Kadavallore, Asha; Walts, Ann E.; Torre, Brian de la; Berel, Dror; Strom, Samuel P.; Aliahmad, Parinaz; Funari, Vincent; Kaye, Jonathan

doi:10.1186/s12885-015-1018-2

Cited by 35 publications

(28 citation statements)

References 56 publications

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“…Therefore, the inhibition of BRCA1 via TOX3 may lead to a series of downstream changes. High expression of TOX3 likely plays a crucial role in breast cancer progression, especially in estrogen receptor-positive mammary epithelial cells (Seksenyan et al, 2015). Therefore, variation in the region regulating TOX3 expression, including rs3803662, is suspected to affect the expression of TOX3, leading to modulation of the BRCA-related breast cancer risk.…”

Section: Discussionmentioning

confidence: 99%

Two polymorphisms, rs2046210 and rs3803662, are associated with breast cancer risk in a Vietnamese case-control cohort

et al. 2018

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Breast cancer is the most common cancer in women worldwide. Breast tumorigenesis encompasses both extrinsic and intrinsic factors. Among intrinsic aspects, the appearance of DNA variation can cause genetic instability, which may lead to carcinogenesis. Genome-wide association studies have found several potential breast cancer-associated single nucleotide polymorphisms (SNPs) in many different populations. Among these, seven (rs2046210, rs1219648, rs3817198, rs3803662, rs889312, rs10941679 and rs13281615) have been shown to be significantly associated with breast cancer risk in various populations including those very similar to the Vietnamese. Here, therefore, we have investigated the relationship between these SNPs and breast cancer risk in a Vietnamese population case-control cohort. Real-time PCR high-resolution melt analysis was performed to genotype 300 breast cancer cases and 325 healthy controls, and the association between the seven SNPs and breast cancer risk was determined by analyzing the differences in allelic and genotypic frequencies between case and control groups using R software. While five of the seven showed no association with breast cancer, there was a relationship between the other two SNPs, rs2046210 and rs3803662, and the risk of developing this disease in Vietnamese women. The A allele is the risk allele for both rs2046210 (OR [95% CI] = 1.43 [1.14 - 1.78], P = 0.0015) and rs3803662 (OR [95% CI] = 1.45 [1.16 - 1.83], P = 0.001). We conclude that two polymorphisms, rs2046210 in ESR1 and rs3803662 in TNRC9, are associated with breast cancer risk in the Vietnamese population.

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Section: Discussionmentioning

confidence: 99%

Two polymorphisms, rs2046210 and rs3803662, are associated with breast cancer risk in a Vietnamese case-control cohort

et al. 2018

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“…Recently, a point of TBX3 regulation has emerged in studies of Tox3 null mice. In normal mice TOX3 is expressed in HS-MECs (based on flow cytometric analysis and ERα, PGR and FOXA1 immunolocalisation [169]) and is able to induce the expression of TBX3 in MCF7 cells.…”

Section: Tbx3mentioning

confidence: 99%

Hormone-Sensing Mammary Epithelial Progenitors: Emerging Identity and Hormonal Regulation

Tarulli

Laven-Law

Shakya

et al. 2015

J Mammary Gland Biol Neoplasia

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The hormone-sensing mammary epithelial cell (HS-MEC-expressing oestrogen receptor-alpha (ERα) and progesterone receptor (PGR)) is often represented as being terminally differentiated and lacking significant progenitor activity after puberty. Therefore while able to profoundly influence the proliferation and function of other MEC populations, HS-MECs are purported not to respond to sex hormone signals by engaging in significant cell proliferation during adulthood. This is a convenient and practical simplification that overshadows the sublime, and potentially critical, phenotypic plasticity found within the adult HS-MEC population. This concept is exemplified by the large proportion (~80 %) of human breast cancers expressing PGR and/or ERα, demonstrating that HS-MECs clearly proliferate in the context of breast cancer. Understanding how HS-MEC proliferation and differentiation is driven could be key to unraveling the mechanisms behind uncontrolled HS-MEC proliferation associated with ERα- and/or PGR-positive breast cancers. Herein we review evidence for the existence of a HS-MEC progenitor and the emerging plasticity of the HS-MEC population in general. This is followed by an analysis of hormones other than oestrogen and progesterone that are able to influence HS-MEC proliferation and differentiation: androgens, prolactin and transforming growth factor-beta1.

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“…TOX2 was reported to play potential roles in reproductive organogenesis [24] and cancer [23]. TOX3 is proved to be involved in the regulation of neuron [25] and oligodendrocyte [26] survival while it also plays multiple roles in breast cancer [27]. TOX4, a platinated-DNA interacting protein, interacts with a complex, controling cell cycle kinetics and chromatin structure [28].…”

Section: Introductionmentioning

confidence: 99%

Clinical characterization, genetic profile, and epigenetic regulation of TOX in diffuse gliomas

Zhang¹,

Fan²,

Yu³

et al. 2020

Preprint

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Background Multiple studies focusing on immune therapy towards glioblastoma (GBM) have attained great successes. TOX has been found to be closely related to immune environment surrounding tumors, while the expression of TOX has not been fully understood in gliomas. Methods Mining data from The Cancer Genome Atlas (TCGA) and the Chinese Glioma Genome Atlas (CGGA), we analyzed 1691 WHO grade I-IV human glioma samples with transcriptome data. R language was used for most statistical analysis. Somatic mutations and somatic copy number variation (CNV) were analyzed using GISTIC 2.0.Results TOX was down-regulated in malignant gliomas, especially in the proneural and isocitrate dehydrogenase (IDH) mutant subtypes of GBM. TOX low tumours are related to loss of PTEN and amplification of EGFR, while TOX high tumours harbor mutations in IDH1 (91%). TOX was highly expressed in cellular tumour, leading edge regions. TOX was enriched in multiple immune related processes including lymphocytes migration in GBM in gene ontology and pathway analysis. Finally, TOX had negative association with the infiltration of several immune cell types in tumour microenvironment in cell lineage analysis. Conclusion TOX has the potential to be a new target for immune-therapy or a prognostic marker for GBM.

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TOX3 is expressed in mammary ER+ epithelial cells and regulates ER target genes in luminal breast cancer

Cited by 35 publications

References 56 publications

Two polymorphisms, rs2046210 and rs3803662, are associated with breast cancer risk in a Vietnamese case-control cohort

Two polymorphisms, rs2046210 and rs3803662, are associated with breast cancer risk in a Vietnamese case-control cohort

Hormone-Sensing Mammary Epithelial Progenitors: Emerging Identity and Hormonal Regulation

Clinical characterization, genetic profile, and epigenetic regulation of TOX in diffuse gliomas

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