Effects of thyroid hormones on human breast cancer cell proliferation

Hall, Linda C.; Salazar, Edmund P.; Kane, Staci R.; Liu, Nan

doi:10.1016/j.jsbmb.2007.12.008

Cited by 147 publications

(128 citation statements)

References 40 publications

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“…It has been shown that T 3 binds and stimulates the estrogen receptor, acting in synergy with estrogen on breast cancer cell lines, potentiating the estrogenic effect, and enhancing cell proliferation (29). The role of estrogen in carcinogenesis of the breast is well known and the possibility that this effect may be even stronger in conjunction with relatively high levels of T 3 could in part explain the results in this study.…”

Section: T 3 (Quartile)supporting

confidence: 60%

Triiodothyronine levels in relation to mortality from breast cancer and all causes: a population-based prospective cohort study

Tosovic

Bondeson

et al. 2013

European Journal of Endocrinology

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Objective: The potential association between thyroid hormones and breast cancer has been investigated in a large number of studies without conclusive results. This study investigated triiodothyronine (T 3 ) levels in relation to breast cancer mortality in a population with no breast cancer patients at baseline. An additional aim was to study T 3 levels in relation to mortality from other cancers and all-cause mortality. Design and methods: This was a population-based prospective cohort study including 2185 women in whom T 3 levels were measured as part of a preventive health project, i.e. before diagnosis in women who later developed breast cancer. Mean follow-up was 24.1 years and record-linkage to The Swedish Cause-of-Death registry identified 471 women who died: 26 out of breast cancer and 182 from other cancers. Mortality was assessed using a Cox's analysis, yielding hazard ratios (HRs), with 95% confidence intervals. Analyses of T 3 as a continuous variable were repeated for pre-and peri/postmenopausal women separately. Results: T 3 levels were positively associated with the risk of breast cancer-specific death in the ageadjusted analysis: HR for T 3 as a continuous variable was 2.80 (1.26-6.25). However, the crude analysis did not reach statistical significance. Breast cancer mortality was even higher in postmenopausal women: 3.73 (1.69-8.22), but stratified analyses included few events. There were no statistically significant associations between T 3 levels and deaths from other cancers, age-adjusted HR: 1.09 (0.72-1.65) or all-cause mortality (1.25:0.97-1.60). Conclusions: This study, the first of its kind on prospectively measured T 3 levels, indicates that T 3 levels are positively associated with breast cancer-specific mortality and that this is not related to a general effect on all-cause mortality.

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Section: T 3 (Quartile)supporting

confidence: 60%

Triiodothyronine levels in relation to mortality from breast cancer and all causes: a population-based prospective cohort study

Tosovic

Bondeson

et al. 2013

European Journal of Endocrinology

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“…In addition, it is well known that the thyroid hormone, as well as estrogens, acts via nuclear receptors, and the mRNA level of the hormone is altered in breast cancer tissues (28). It is also known that thyroid hormone receptors bind to an estrogen response element of target gene promoters, which affects the estrogen-dependent gene transcription (29). A study on breast cancer cell lines have revealed that the thyroid hormone stimulates cell growth and division in the ER-positive MCF-7 cell line (30).…”

Section: Rt-qpcr Evaluations On Human Breast Cancer and Non-cancerousmentioning

confidence: 99%

Comparison of the seleno-transcriptome expression between human non-cancerous mammary epithelial cells and two human breast cancer cell lines

et al. 2017

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Abstract. Breast cancer is the second most common cause of mortality in women; therefore, the identification of novel putative markers is required to improve its diagnosis and prognosis. Selenium is known to protect mammary epithelial cells from oxidative DNA damage, and to inhibit the initiation phase of carcinogenesis by stimulating DNA repair and apoptosis regulation. Consequently, the present study has focused attention on the selenoprotein family and their involvement in breast cancer. The present study performed a global analysis of the seleno-transcriptome expression in human breast cancer MCF-7 and MDA-MB231 cell lines compared with healthy breast MCF-10A cells using reverse transcription-quantitative polymerase chain reaction. The present data revealed the presence of differently expressed genes in MCF-7 and MDA-MB231 cells compared with MCF-10A cells: Four downregulated [glutathione peroxidase (GPX)1, GPX4, GPX5 and GPX7] and three upregulated (deiodinase iodothyronine, type II, GPX2 and GPX3) genes. Additionally, interactomic investigation were performed by the present study to evaluate the association between the downregulated and upregulated genes, and to identify putative HUB nodes, which represent the centers of association between the genes that are capable of direct control over the gene networks. Network analysis revealed that all differentially regulated genes, with the exception of selenoprotein T, are implicated in the same network that presents three HUB nodes interconnected to the selenoprotein mRNAs, including TP53, estrogen receptor 1 and catenin-β1 (CTNNB1). Overall, these data demonstrated for the first time, a profile of seleno-mRNAs specific for human breast cells, indicating that these genes alter their expression on the basis of the ER-positivity or negativity of breast cancer cells.

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“…Besides their suppressor role, TRs enhanced tumor progression in other studies. Thyroid hormones stimulate the proliferation of several cancer cell types including those from the pituitary (Barrera-Hernandez et al, 1999), gliomas (Davis et al, 2006), breast cancers (Hall et al, 2008) and prostate cancers (Tsui et al, 2008). Thyroid hormone and the TRa1 receptor control epithelial cell proliferation and the expression of components of the Wnt pathway (Plateroti et al, 2006).…”

Section: Trb1mentioning

confidence: 99%

Cathepsin H regulated by the thyroid hormone receptors associate with tumor invasion in human hepatoma cells

Huang

Yeh

et al. 2011

Oncogene

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Thyroid hormone, 3, 3 0 , 5-triiodo-L-thyronine (T 3 ), mediates cell growth, development and differentiation by binding to its nuclear receptors (TRs). The role of TRs in cancer is still undefined. Notably, hyperthyroxinemia has been reported to influence the rate of colon cancer in an experimental model of carcinogenesis in rats. Previous microarray analysis revealed that cathepsin H (CTSH) is upregulated by T 3 in HepG2-TR cells. We verified that mRNA and protein expression of CTSH are induced by T 3 in HepG2-TR cells and in thyroidectomized rats following administration of T 3 . The possible thyroid hormone-responsive elements of the CTSH promoter localized to the nucleotides -2038 to -1966 and -1565 to -1501 regions. An in vitro functional assay showed that CTSH can increase metastasis. J7 cells overexpressing CTSH were inoculated into severe combined immunedeficient mice and these J7-CTSH mice displayed a greater metastatic potential than did J7-control mice. The clinicopathologic significance of CTSH expression in hepatocellular carcinoma (HCC) was also investigated. The CTSH overexpressing in HCC was associated with the presence of microvascular invasion (P ¼ 0.037). The microvascular invasion characteristic is closely related to our in vitro characterization of CTSH function. Our results show that T 3 -mediated upregulation of CTSH led to matrix metallopeptidase or extracellular signal-regulated kinase activation and increased cell migration. This study demonstrated that CTSH overexpression in a subset hepatoma may be TR dependent and suggests that this overexpression has an important role in hepatoma progression.

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Effects of thyroid hormones on human breast cancer cell proliferation

Cited by 147 publications

References 40 publications

Triiodothyronine levels in relation to mortality from breast cancer and all causes: a population-based prospective cohort study

Triiodothyronine levels in relation to mortality from breast cancer and all causes: a population-based prospective cohort study

Comparison of the seleno-transcriptome expression between human non-cancerous mammary epithelial cells and two human breast cancer cell lines

Cathepsin H regulated by the thyroid hormone receptors associate with tumor invasion in human hepatoma cells

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