Thyroid Hormone Receptor α1 Directly Controls Transcription of the β-Catenin Gene in Intestinal Epithelial Cells

Plateroti, Michelina; Kress, Elsa; Mori, Jun; Samarut, Jacques

doi:10.1128/mcb.26.8.3204-3214.2006

Cited by 117 publications

(132 citation statements)

References 52 publications

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“…However, elucidation of the underlying mechanisms by which T 3 regulated requires further study. Previous reports have shown that TRs are potent inducer of tumorigenesis (Plateroti et al, 2006;Chen et al, 2008a;Kress et al, 2009). In this study, we report that the T 3 /TR controls the transcription of the CTSH gene and that T 3 -mediated cell migration appears to involve CTSH.…”

Section: Trb1mentioning

confidence: 49%

“…Thyroid hormone and TRa1 control epithelial cell proliferation and the expression of components of the Wnt pathway (Plateroti et al, 2006). The expression of the b-catenin and sFRP2 gene is regulated directly by TRa1, and the Wnt/ b-catenin signaling networks contribute to intestinal tumorigenesis (Kress et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…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%

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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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Section: Trb1mentioning

confidence: 49%

Section: Discussionmentioning

confidence: 99%

Section: Trb1mentioning

confidence: 99%

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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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“…The synthetic (-)-agelastatin A (15, 16) that we used in this study was shown to inhibit OPN protein expression in part through its potent modulatory effects on two components of the Wnt signaling pathway, that is, h-catenin and Tcf-4, although precisely how (-)-agelastatin A modulates these two Wnt effector proteins still remains unclear. Genes already known or suspected to have a down-regulatory effect on h-catenin-mediated signaling include APC, axin (40), conductin/axil, y-TRCP (41), DAPPER (42), NOTCH1 (43), PPA2 (44), presenilin (40), TLE/Groucho, TSC1/2 (45), tuberin-hamartin (46), thyroid hormone receptor (47), and p300/CRBP (48). Genes thus far implicated in regulating Tcf-4 levels include the Nemo-like kinase ring finger protein, NARF (which regulates ubiquitination and degradation of Tcf/Lef), and the Fgf15 gene.…”

Section: Discussionmentioning

confidence: 99%

Agelastatin A: a novel inhibitor of osteopontin-mediated adhesion, invasion, and colony formation

Mason

McFarlane

Johnston

et al. 2008

Molecular Cancer Therapeutics

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Effective inhibitors of osteopontin (OPN) -mediated neoplastic transformation and metastasis are still lacking. (-)-Agelastatin A is a naturally occurring oroidin alkaloid with powerful antitumor effects that, in many cases, are superior to cisplatin in vitro . In this regard, past comparative assaying of the two agents against a range of human tumor cell lines has revealed that typically (-)-agelastatin A is 1.5 to 16 times more potent than cisplatin at inhibiting cell growth, its effects being most pronounced against human bladder, skin, colon, and breast carcinomas. In this study, we have investigated the effects of (-)-agelastatin A on OPN-mediated malignant transformation using mammary epithelial cell lines. Treatment with (-)-agelastatin A inhibited OPN protein expression and enhanced expression of the cellular OPN inhibitor, Tcf-4. (-)-Agelastatin A treatment also reduced B-catenin protein expression and reduced anchorage-independent growth, adhesion, and invasion in R37 OPN pBK-CMV and C9 cell lines. Similar effects were observed in MDA-MB-231 and MDA-MB-435s human breast cancer cell lines exposed to (-)-agelastatin A. Suppression of Tcf-4 by RNA interference (short interfering RNA) induced malignant/invasive transformation in parental benign Rama 37 cells; significantly, these events were reversed by treatment with (-)-agelastatin A. Our study reveals, for the very first time, that (-)-agelastatin A down-regulates B-catenin expression while simultaneously up-regulating Tcf-4 and that these combined effects cause repression of OPN and inhibition of OPN-mediated malignant cell invasion, adhesion, and colony formation in vitro. We have also shown that (-)-agelastatin A inhibits cancer cell proliferation by causing cells to accumulate in the G 2 phase of cell cycle.

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“…This function depends on the TR 1 receptor Plateroti et al, 2001;Flamant et al, 2002) and involves the transcriptional regulation of cell cycle control genes and of the Wnt/ -catenin pathway (Plateroti et al, 2006;Kress et al, 2009) (detailed in the next paragraph);…”

Section: Data From Engineered Micementioning

confidence: 99%

Thyroid hormones and the control of cell proliferation or cell differentiation: Paradox or duality?

Kress

Samarut

Plateroti

2009

Molecular and Cellular Endocrinology

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Thyroid hormones and the control of cell proliferation or cell differentiation: paradox or duality?. Molecular and Cellular Endocrinology, Elsevier, 2009, 313 (1-2) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. SummaryAmphibian metamorphosis perfectly illustrates a key paradox: thyroid hormones control diverse cellular processes depending on the tissue context. This point is also reinforced by a recent accumulation of evidence. For example, thyroid hormones and their nuclear receptor TRs have been described to function in different systems in synergy and/or in antagonism with other signaling pathways. This interaction helps explain their pleiotropic roles. This review summarizes the most important advances in this field, focusing in particular on the key action of thyroid hormones in controlling the balance between the processes of cell proliferation and cell differentiation in a few organs, with special attention paid to the intestine. We highlight similarities between the cellular and molecular events occurring during postnatal intestinal maturation at metamorphosis in amphibians, and comparable events observed at weaning in mice. 1-Introduction1.1 Thyroid hormone production Thyroid hormones (THs), L-thyroxine or T4 and 3,5,3'-L-triiodothyronine or T3, are essential for the development of several organs, including the central nervous system, skeleton, heart, intestine, skeletal muscle and sensory organs. Moreover, they also have important regulatory effects on oxygen consumption and metabolic rate (Oppenheimer et al., 1987). The follicular cells of the thyroid gland synthesize and secrete both hormones, but T4 is the most abundant. This process is under the control of circulating THs levels through the hypothalamuspituitary-thyroid feedback regulatory loop (rev. in Fredric and Wondisford, 2004). The intracellular concentration of T3 is dependent upon the uptake of T3 and T4, and their subsequent metabolism (Bianco and Kim, 2006). In fact, both hormones are actively transported across the cell membrane by specific transporter proteins, of which monocarboxylate transporter-8 is the best characterized (Dumitrescu et al., 2004;Friesema et al., 2004; rev. in Refetoff andDumitrescu, 2007 andVisser et al., 2007). Three iodothyronine deiodinase selenoenzymes (D1, D2 and D3) regulate TH activation and catabolism (Bianco and Kim, 2006). D1 and D2 catalyze the 5'-deiodination of T4 to its active metabolite T3. T3 is generated from the activity of D1, which is the main source of circulating T3. In contrast, D2 is the isoenzyme primarily responsible for local production of T3 in target cells. T3 derived from ...

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Thyroid Hormone Receptor α1 Directly Controls Transcription of the β-Catenin Gene in Intestinal Epithelial Cells

Cited by 117 publications

References 52 publications

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

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

Agelastatin A: a novel inhibitor of osteopontin-mediated adhesion, invasion, and colony formation

Thyroid hormones and the control of cell proliferation or cell differentiation: Paradox or duality?

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