Transformation of estrone and estradiol in hormone-dependent and hormone-independent human breast cancer cells

Nguyen, B.-L.; Chétrite, G.; Pasqualini, Jörge R.

doi:10.1007/bf00665786

Cited by 44 publications

(22 citation statements)

References 32 publications

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“…Progestins have been shown to inhibit the reductive 17␤-HSD activity as well as to stimulate the oxidative 17␤-HSD activity, respectively in BC cell lines. In contrast, sulfotransferase activity was shown to be increased in MCF-7 and T-47D cell lines when progestins were added [32,41,60,61]. A recent study in BC cells demonstrated different effects on various enzymes depending on what type of progestin and estradiol was combined with [44].…”

Section: Discussionmentioning

confidence: 96%

“…Thus, STS seems to play a crucial role in local biosynthesis of estrogens in breast (cancer) tissue. Estradiol and various progestogens have been shown to influence STS in BC cells in vitro [38][39][40][41][42][43][44]. In vitro, the effect of steroids on local estrogen formation in normal and malignant breast cells is rather due to changes in STS activity than in its mRNA and protein levels [45].…”

Section: Introductionmentioning

confidence: 99%

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Effects of black cohosh on estrogen biosynthesis in normal breast tissue in vitro

Stute¹,

Nisslein

Götte³

et al. 2007

Maturitas

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Objectives: To investigate the effect of black cohosh on the estrogen biosynthesis in the breast in vitro. Methods: Steroid sulfatase (STS) activity was studied in normal breast tissue obtained from pre-and postmenopausal women undergoing reduction mammoplasty. STS protein expression was studied by immunohistochemistry and western blotting. Breast tissue was incubated in vitro without or with black cohosh (iCR) at concentrations ranging from 0.1 mg/ml to 1 ng/ml. STS activity was evaluated by incubating homogenized breast tissue with [ 3 H]-estrone sulfate, separating the formed products, estrone (E 1 ) and estradiol (E 2 ), by thin layer chromatography and measuring the amounts of E 1 and E 2 by scintillation counting. Results: STS protein expression and enzymatic activity were detected in all specimens investigated. In all groups, significantly more E 1 than E 2 was produced. Local estrogen formation was decreased in premenopausal breast tissue by treatment with iCR at 0.1 mg/ml (p ≤ 0.05). Conclusions: iCR decreases local estrogen formation in normal human breast tissue in vitro. This may contribute to the lack of hormonal effects of black cohosh in breast tissue observed in previous studies.

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Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 99%

Effects of black cohosh on estrogen biosynthesis in normal breast tissue in vitro

Stute¹,

Nisslein

Götte³

et al. 2007

Maturitas

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“…as such, modulation of the receptor status may coincide with progression of hormone-dependent tumours to a hormoneindependent status (Abul-Hajj, 1979;McCormick et al, 1982;Prudhomme et al, 1984;Welsch, 1985Welsch, , 1987Mauvais-Jarvis et al, 1986;Siiteri et al, 1986;Ball et al, 1988;Castagnetta et al, 1995;Nguyen et al, 1995). In this context, it is interesting to note that MMEC/mnvc3 cells that express exogenous c-m!yc also exhibit about a 60% decrease in oestrogen receptor content relative to the parental MMEC cells.…”

Section: Discussionmentioning

confidence: 99%

Alteration of oestradiol metabolism in myc oncogene-transfected mouse mammary epithelial cells

Telang

Arcuri²,

Granata³

et al. 1998

Br J Cancer

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Summary Targeted overexpression of the c-myc oncogene induces neoplastic transformation in immortalized, non-tumorigenic mouse mammary epithelial cells (MMEC). Experiments in the present study were conducted to examine whether cellular transformation induced by c-myc oncogene is associated with altered metabolism of 17,-oestradiol (E2). The Keywords: c-myc expression; oestradiol metabolism; mammary carcinogenesis It is well recognized that oestrogens exert a profound influence on mammary epithelial cell growth, differentiation and neoplastic transformation Prudhomme et al, 1984;Mauvais-Jarvis et al, 1986;Siiteri et al, 1986). The molecular and biochemical mechanisms important for oestrogen responsiveness and the influence of altered oestrogen responsiveness on mammary cell carcinogenesis, however, are not fully understood. Our earlier studies on immortalized, non-tumorigenic mouse mammary epithelial cell lines have shown that transfection of the cell line with myc or Ras oncogenes results in neoplastic transformation. Before tumorigenesis in vivo, myc as well as Ras transfectants exhibit aberrant hyperproliferation in vitro (Telang et al, 1990(Telang et al, , 1991Suto et al, 1992). Thus, persistent oncogene expression and aberrant hyperproliferation may represent molecular and cellular biomarkers for neoplastic transformation.The conventionally recognized markers for oestrogen responsiveness include (1) functional activity of oestrogen receptor as determined by receptor-ligand binding; (2) modulation of transcriptional activity, growth and induction of progesterone receptor (Prudhomme et al, 1984;Mauvais-Jarvis et al, 1986;Siiteri et al, 1986;Dubik and Shiu, 1992); (3) (Telang et al, 1991Suto et al, 1993). In addition, it has been proposed that the oestrogenmediated stimulation of growth of breast tumour-derived MCF7 cells may involve transactivation in the c-mvc promoter region (Dubik and Shiu, 1992). It is not clear whether these molecular and metabolic alterations characterize the initiated phenotype or represent a late-occurring, post-initiational event in a rapidly growing tumour cell phenotype.The experiments in the present study were designed to (1) establish the validity of oestrogen metabolism as an endocrine biomarker for tumorigenic transformation in mnyc oncogene-transfected mammary epithelial cells; and (2) elucidate the relationship between myc expression, the extent of cellular metabolism of E, and tumorigenic transformation. To this end, we have compared the extent of EB metabolism in the spontaneously immortalized, non-tumorigenic mammary epithelial cell line MMEC and the stable transfectant MMEC/myc3 that expresses activated c-myc proto-oncogene and is highly tumorigenic.1549

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“…HSD17B1 (17b-hydroxysteroid dehydrogenase1) is the most active enzyme to produce E2 [7][8][9][10] and significantly overexpressed in breast cancer, which contributes to the stimulation and development of breast cancer., 11,12 HSD17B2, which converts E2 to E1, is dominant in normal breast. 13 Studies have shown that increased HSD17B1 expression or ratio of HSD17B1 and HSD17B2 expression is associated with poor clinical outcome of estrogen-dependent breast cancer patients. 12,14 Besides HSD17B1, HSD17B7 has been identified as a key enzyme for the viability of breast cancer due to the dual functions on activation and reduction of estrogen and androgen.…”

Section: Introductionmentioning

confidence: 99%

Acetylation targets HSD17B4 for degradation via the CMA pathway in response to estrone

Zhang

Yao

et al. 2017

Autophagy

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Dysregulation of hormone metabolism is implicated in human breast cancer. 17b-hydroxysteroid dehydrogenase type 4 (HSD17B4) catalyzes the conversion of estradiol (E2) to estrone (E1), and is associated with the pathogenesis and development of various cancers. Here we show that E1 upregulates HSD17B4 acetylation at lysine 669 (K669) and thereby promotes HSD17B4 degradation via chaperonemediated autophagy (CMA), while a single mutation at K669 reverses the degradation and confers migratory and invasive properties to MCF7 cells upon E1 treatment. CREBBP and SIRT3 dynamically control K669 acetylation level of HSD17B4 in response to E1. More importantly, K669 acetylation is inversely correlated with HSD17B4 in human breast cancer tissues. Our study reveals a crosstalk between acetylation and CMA degradation in HSD17B4 regulation, and a critical role of the regulation in the malignant progression of breast cancer.

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Transformation of estrone and estradiol in hormone-dependent and hormone-independent human breast cancer cells

Cited by 44 publications

References 32 publications

Effects of black cohosh on estrogen biosynthesis in normal breast tissue in vitro

Effects of black cohosh on estrogen biosynthesis in normal breast tissue in vitro

Alteration of oestradiol metabolism in myc oncogene-transfected mouse mammary epithelial cells

Acetylation targets HSD17B4 for degradation via the CMA pathway in response to estrone

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