Regulation of sex steroid formation by interleukin-4 and interleukin-6 in breast cancer cells

Turgeon, Carl; Gingras, Sébastien; Carrière, Marie-Claude; Blais, Yves; Labrie, Fernand; Simard, Jacques

doi:10.1016/s0960-0760(98)00031-4

Cited by 31 publications

(19 citation statements)

References 61 publications

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“…It has been recently demonstrated that mammary tissue possesses these activating enzymes for DHEA or androstenedione (Belvedere et al 1996); thus, the mammary gland can be considered a site for the synthesis of active androgens. Our data on HC11 cell growth support the hypothesis that local intracrine formation of androgenic steroids from precursors may play a role in the regulation of growth and function of the mammary gland (Recchione et al 1995, Turgeon et al 1998. The ability to block the effect of androgens using AR antagonists provides further support that the effect is specific.…”

Section: Discussionsupporting

confidence: 76%

Role of androgens in proliferation and differentiation of mouse mammary epithelial cell line HC11

Baratta

Grolli²,

Poletti

et al. 2000

Journal of Endocrinology

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Androgens have been found in mammary epithelium and in milk throughout the cycle of the mammary gland in vivo. The aim of this study was to investigate the possible role of these substances in mammary epithelial growth and differentiation in the mouse HC11 cell line. Cells were stimulated with testosterone, dihydrotestosterone, androstenedione and 5 -androstane-3 ,17 -diol at concentrations ranging between 0·3 nM and 30 nM. Cyproterone acetate or flutamide, androgen receptor antagonists, (3 µM) were used to block specific androgen effects. Proliferative effects were measured by an MTT (tetrazolium blue) conversion test and [ 3 H]thymidine uptake. HC11 cells were transfected with p cCAT, a chimeric rat -casein gene promoter-chloramphenicol acetyl transferase (CAT) gene construct and CAT ELISA was used to determine gene expression. RT-PCR was performed to detect androgen receptor expression. After 24, 48 and 72 h androgens significantly (P<0·05) increased proliferation. Androgen antagonists significantly (P<0·05) reduced the proliferative effects. Furthermore androgens potentiated the lactogenic effect of prolactin, insulin and dexamethasone (P<0·05). Finally, the androgen receptor gene was expressed in both proliferating and differentiated HC11 cells. These observations lead us to hypothesize an activity of this class of steroids in mammary physiology. In particular, androgens stimulate cell proliferation and -casein gene expression; this influence appears to be mediated by androgen receptors.

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Section: Discussionsupporting

confidence: 76%

Role of androgens in proliferation and differentiation of mouse mammary epithelial cell line HC11

Baratta

Grolli²,

Poletti

et al. 2000

Journal of Endocrinology

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“…In addition, we previously reported that expression levels of in situ estrogen synthesizing and/or metabolizing enzymes may be significantly associated with the degree of atherosclerotic changes in female aorta, which may be related to cytokines produced in situ in human atherosclerotic lesions [10]. Previous reports also documented that some cytokines and hormones were involved in regulation of 3b-HSD expression in breast cancer and/or testis [17,18]. These may explain an association between 3b-HSD expression and degrees of atherosclerotic changes in human aorta.…”

Section: Discussionmentioning

confidence: 94%

“…The SUPERSCRIPT Preamplification system RT kit (Gibco-BRL, Grand Island, NY) was employed in the synthesis and amplification of complementary DNA (cDNA). cDNA was synthesized from total RNA (2 mg) using 25 ng/mL Oligo (dT) [12][13][14][15][16][17][18] Primer (Life Technologies, Inc., Gaithersburg, MD) on a PTC-200 Peltier Thermal Cycler DNA Engine (MJ Research, Inc., Watertown, MA). In order to test the presence of genomic DNA contamination, we performed the RT step in the absence of SUPERSCRIPT TM II RNase H -Reverse Transcriptase (Gibco-BRL) followed by PCR.…”

Section: Real-time Polymerase Chain Reaction (Pcr)mentioning

confidence: 99%

3β-Hydroxysteroid Dehydrogenase in Human Aorta

et al. 2005

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Abstract. 3b-hydroxysteroid dehydrogenase (3b-HSD) is known to be involved in steroid production and/or metabolism and to be expressed in many tissues including adrenal cortex. Expression of this enzyme has also been elucidated in human cardiovascular system but its details remain largely unknown. Therefore, in this study, we examined the status of 3b-HSD in postmortem human aorta utilizing RT-PCR and immunohistochemical analysis. Both mRNAs and immunoreactivity for the enzyme were detected predominantly in female aorta, and in those with mild atherosclerotic changes. In addition, immunohistochemical study demonstrated that immunoreactivity for 3b-HSD was detected in vascular smooth muscle cells (VSMCs) of aorta. These findings all indicated that steroidogenesis via 3b-HSD may occur in VSMCs of human aorta, possibly related to gender differences and/or the degree of atherosclerosis.

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“…Enzyme assays. The modified assay procedures for 5␣-reductase and for 17␤-hydroxysteroid dehydrogenase (17␤-HSD) oxidative and reductive activities have been described in detail previously (1,37,48). The assay mixtures after the enzyme reaction were extracted five times with methylene chloride, and the steroids in the organic phase were analyzed by thin-layer chromatography (TLC) using the mobile phase of chloroform-ethyl acetate (3:1, vol/vol).…”

Section: Chemicalsmentioning

confidence: 99%

Mechanism for normal splenic T lymphocyte functions in proestrus females after trauma: enhanced local synthesis of 17β-estradiol

Samy

Zheng

Matsutani

et al. 2003

American Journal of Physiology-Cell Physiology

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and resuscitation (TH) produces profound immunodepression and enhances susceptibility to sepsis in males but not in proestrus females, suggesting gender dimorphism in the immune responses. However, the mechanism responsible for the maintenance of immune functions in proestrus females after TH is unclear. Splenic T lymphocytes express receptors for estrogen (ER), contain enzymes involved in estrogen metabolism, and are the major source of cytokine production; the metabolism of 17␤-estradiol was assessed in the splenic T lymphocytes of proestrus and ovariectomized mice by using appropriate substrates after TH. Analysis for aromatase and 17␤-hydroxysteroid dehydrogenases indicated increased 17␤-estradiol synthesis and low conversion into estrone in T lymphocytes of proestrus but not of ovariectomized mice. The effect of 17␤-estradiol on T lymphocyte cytokine release was reliant on ER expressions. This was apparent in the differences of ER expression, especially that of ER-␤, and an association between increased 17␤-estradiol synthesis and sustained release of IL-2 and IL-6 in T lymphocytes of proestrus females after TH. Because 17␤-estradiol is able to regulate cytokine genes, and the splenic T lymphocyte cytokine releases is altered after TH, continued synthesis of 17␤-estradiol in proestrus females appears to be responsible for the maintenance of T lymphocyte cytokine release associated with the protection of immune functions after TH. inflammation; immune suppression; steroid synthesis; T lymphocytes; cytokines THE INFLUENCE OF GENDER on immune functions has been recognized for many years, and in general, women are known to develop enhanced humoral responses compared with men and are more prone to autoimmune diseases (9,12,20). Trauma-hemorrhage and resuscitation (TH) produce severe impairment of both immune and cardiovascular functions (51,56,57). Although depression of cellular immunity occurs very early following TH, the loss in immune functions persists for a prolonged period, which may lead to subsequent sepsis with high mortality rates (43, 56). The immune depression is pronounced in males and ovariectomized females (OVX) after TH compared with proestrus females (54, 55). Moreover, immune functions in males and OVX females can be restored by the administration of 17␤-estradiol (E2) after TH (16-18). Thus gender dimorphism is obvious in the loss of immune functions after TH, implicating a major role for sex steroid hormones (2, 4).Steroid hormones regulate immune functions in vivo, and the mechanisms involve not only the control of cytokine gene transcription by the classic steroid hormone-receptor complex but also the tissue-specific metabolism of sex steroids (11,21,24,29,33,36,47). Among the sex steroids, estrogen is demonstrated to protect immune functions after TH because proestrus females are not immunodepressed compared with male and OVX mice. Furthermore, the depressed immune functions in males and OVX females after TH can be normalized by parenteral E2 administration (16-18). The ovary is the prima...

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Regulation of sex steroid formation by interleukin-4 and interleukin-6 in breast cancer cells

Cited by 31 publications

References 61 publications

Role of androgens in proliferation and differentiation of mouse mammary epithelial cell line HC11

Role of androgens in proliferation and differentiation of mouse mammary epithelial cell line HC11

3β-Hydroxysteroid Dehydrogenase in Human Aorta

Mechanism for normal splenic T lymphocyte functions in proestrus females after trauma: enhanced local synthesis of 17β-estradiol

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Regulation of sex steroid formation by interleukin-4 and interleukin-6 in breast cancer cells

Cited by 31 publications

References 61 publications

Role of androgens in proliferation and differentiation of mouse mammary epithelial cell line HC11

Role of androgens in proliferation and differentiation of mouse mammary epithelial cell line HC11

3&beta;-Hydroxysteroid Dehydrogenase in Human Aorta

Mechanism for normal splenic T lymphocyte functions in proestrus females after trauma: enhanced local synthesis of 17β-estradiol

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3β-Hydroxysteroid Dehydrogenase in Human Aorta