Antiestrogens prevent the stimulatory effects of L-triiodothyronine on cell proliferation

Zhou-Li, Fei

doi:10.1210/en.130.3.1145

Cited by 27 publications

(22 citation statements)

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“…TR are also present in human breast cancer cell lines (Burke and McGuire, 1978;Zhou-Li et al, 1992), but con¯icting reports describe both mitogenic and antimitogenic e ects of T3 (Nogueira and Brentani, 1996;MartõÂ nez et al, 2000). A role of T3 in the physiology of ®brocystic breast disease has been suggested (MartõÂ nez et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

Expression of thyroid hormone receptor/erbA genes is altered in human breast cancer

et al. 2002

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The relation between thyroid status and diseases and cancer is unclear. No detailed analysis of thyroid hormone receptor (TR) expression in human breast cancer has been reported. We have analysed the expression and mutational status of the TRa1, encoded by the c-erbA proto-oncogene, TRb1 and TRb2 isoforms in 70 sporadic breast cancers. Alterations in the RNA level of TRb1, TRa1, or both were found in a number of patients. No expression of TRb2 RNA was detected. Western blotting analysis con®rmed the di erences in expression at the protein level in those cases where su cient tumor sample was available. Additionally, tumor-speci®c truncated TRb1 RNA was found in six patients. Strikingly, three transcripts shared the same breakpoint. Only one tumor carried the corresponding deletion at the genomic DNA level, suggesting that the remaining abnormal TRb1 transcripts are aberrant splicing products. Though no signi®cant correlation was found between TRb1 alteration and any clinical parameter, it showed a tendency to associate with early age of onset (550 years). Our results reveal speci®c alterations in the expression of TRb and TRa genes in a subset of breast cancer patients, suggesting that deregulation of thyroid hormone target genes may be involved in the generation of this neoplasia.

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Section: Discussionmentioning

confidence: 99%

Expression of thyroid hormone receptor/erbA genes is altered in human breast cancer

et al. 2002

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“…Manipulations of thyroid hormones and estrogen in vitro potentiate or mutually inhibit effects on gene expression (2)(3)(4). Our data presented in the accompanying paper (5) demonstrates that both TRs and ERs are present in rat hypothalamic nuclear extracts and both can bind to a preproenkephalin (PPE) promoter ERE.…”

mentioning

confidence: 93%

Thyroid hormone and estrogen interact to regulate behavior.

Dellovade

Zhu

Krey

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

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Environmental perturbations that increase plasma thyroid hormone (T3) concentrations also profoundly affect female reproductive behavior and physiology. We explored whether these effects were mediated by interactions between T3 receptor (TR) and estrogen receptor (ER (6)(7)(8)(9). Decreased ambient temperature can delay puberty in juveniles, and inhibit ovulation, decrease sexual behavior, alter gonadotropin release, and decrease litter size in adults (10-12). Thus, changes in serum thyroid hormone concentrations might be important for signaling environmental conditions to neuroendocrine mechanisms, conceivably by interactions of TRs with ERs on hormone response elements of relevant genes (13). The neural circuitry involved in lordosis, a female rat sexual behavior, is relatively well-understood and is known to be mediated by estrogen acting via hypothalamic ERs (14). However, interactions between thyroid hormones and estrogen on reproductive behavior have not been studied. MATERIALS AND METHODSAnimals and Experimental Design. In the first experiment, we asked whether altered plasma thyroid hormone levels would affect EB-induced lordosis behavior. We used both OVX and thyroidectomized/ovariectomized (TX/OVX) Sprague Dawley rats for this study. We gave daily low doses of EB (2 ,ug, s.c.) to slowly increased plasma estradiol (E2) concentrations in OVX rats, thereby gradually increasing sexual receptivity. T3 was given in high doses (500 ,ug per kg body weight, i.p.) to OVX females to induce hyperthyroid plasma concentrations. In contrast, lower doses of T3 (20 ,ug per kg body weight, i.p) were given to TX/OVX females to increase plasma concentrations within the physiological range.Two weeks after surgery, OVX rats (175-225 g) were treated daily for 10 days with vehicle (n = 13), EB (2 ,g, s.c.; n = 13), high doses of T3 (500 ,ug per kg body weight, i.p.; n = 13), or EB + high doses of T3 (n = 15). TX/OVX females were treated daily for 10 days with vehicle (n = 14), EB (2 ,g; n = 16), low doses of T3 (20 jig per kg body weight i.p.; n = 13), or low doses of T3 + EB (n = 15). T3 was administered every 12 hr at 9:00 a.m. and 9:00 p.m., and EB was injected once a day at 9:00 a.m. In both experiments, animal surgeries were performed by the supplier (Charles River Breeding Laboratories) and animals were maintained on a 12-hr light/12-hr dark cycle (lights on at 7:00 p.m.). Food and water were

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“…Studies over the past decade have demonstrated marked functional crosstalk between receptor systems (Bunone et al 1996). In this respect, tri-iodothyronine (T 3 )-induced growth of GH 3 cells has been shown to be inhibited by antioestrogens (Zhou-Li et al 1992). Similarly, the synthetic glucocorticoid, dexamethasone (Dex), has been shown to inhibit both oestrogen-and T 3 -induced growth of GH 3 cells (Zhou-Li et al 1991).…”

Section: Introductionmentioning

confidence: 99%

Dexamethasone blocks antioestrogen- and oxidant-induced death of pituitary tumour cells

Newton¹,

bilko²,

Pappa³

et al. 2001

Journal of Endocrinology

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The oestrogen receptor is fundamental to the growth and survival of the rat pituitary tumour cell line, GH 3 . Our previous studies have shown that antioestrogens such as RU 58668 and ZM 182780 will reduce the rate of cell division and also induce cell death. Death of these cells in response to antioestrogen treatment appears to be due to a heightened sensitivity to reactive oxygen species (ROS). As part of a study to determine the cross-talk between steroid receptor systems in these cells, we have observed that the glucocorticoid, dexamethasone (Dex), inhibits antioestrogen-induced cell death. Cell death induced by H 2 O 2 is enhanced by ZM 182780 and this effect is also blocked by Dex. As apoptotic cell death in a number of systems involves an early loss of mitochondrial membrane potential ( m ), we have performed detailed studies on the time-course of m loss in relation to the loss in cell membrane function. These studies have indicated that a loss of m parallels a loss of cell membrane functionthis is more characteristic of necrosis than of apoptosis.From microscopic observations of these cells in response to H 2 O 2 , it has been noted that early cell membrane blebbing, induced by H 2 O 2 , is blocked in the presence of ZM 182780. Cell membrane blebbing can precede necrosis as well as apoptosis and it is thought to involve cytoskeletal changes, for which localised glycolytic reactions provide ATP. These observations, together with those showing that removal of glucose, but not inhibition of mitochondrial function, enhances ROS-induced cell death, prompted studies on the glycolytic pathway. As a strong candidate mechanism, it would appear that, via an effect on one of the rate-limiting glycolytic enzymes, glyceraldehyde-3-phosphate dehydrogenase, Dex is able to overcome the antioestrogen-enhanced loss of glycolytic function following exposure of cells to ROS. This report contributes to the growing body of evidence showing that glucocorticoids provide a survival advantage to both normal and tumour cell types.

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Antiestrogens prevent the stimulatory effects of L-triiodothyronine on cell proliferation

Cited by 27 publications

References 0 publications

Expression of thyroid hormone receptor/erbA genes is altered in human breast cancer

Expression of thyroid hormone receptor/erbA genes is altered in human breast cancer

Thyroid hormone and estrogen interact to regulate behavior.

Dexamethasone blocks antioestrogen- and oxidant-induced death of pituitary tumour cells

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