Molecular expression of 17βhydroxysteroid dehydrogenase types in relation to their activity in intact human prostate cancer cells

Carruba, Giuseppe; Adamski, Jerzy; Calabrò, Maurizio; Miceli, M; Cataliotti, Antonella; Bellavia, Vincenzo; Bue, A. Lo; Polito, Lucia M.; Castagnetta, L.

doi:10.1016/s0303-7207(97)00092-0

Cited by 21 publications

(13 citation statements)

References 22 publications

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“…Also known as peroxisomal multifunctional enzyme type 2, or D-bifunctional protein, 17-h-HSD4 is an enzyme that inactivates estradiol by conversion to estrone and participates in peroxisomal h-oxidation of fatty acids. With 17-h-HSD4 highly expressed in prostate and testis, differential expression of 17-h-HSD enzymes is associated with the endocrine status of prostate cancer cells and dependent pathways of estrogen metabolism (27). In addition to being a major enzyme in the biosynthesis of sex hormones, 17-h-HSD4 is implicated in LOX metabolism: mutations in this gene are associated with a developmental neurologic disorder with the increased degradation of leukotrienes (28).…”

Section: Cancer Researchmentioning

confidence: 99%

Distinct Effects of Annexin A7 and p53 on Arachidonate Lipoxygenation in Prostate Cancer Cells Involve 5-Lipoxygenase Transcription

et al. 2006

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Tumor suppressor function for Annexin A7 (ANXA7; 10q21) is based on cancer-prone phenotype in Anxa7(+/À) mouse and ANXA7 prognostic role in human cancers. Because ANXA7-caused liposome aggregation can be promoted by arachidonic acid (AA), we hypothesized that the phospholipid-binding tumor suppressor ANXA7 is associated with AA cascade. In a comparative study of ANXA7 versus canonical tumor suppressor p53 effects on AA lipoxygenation pathway in the p53-mutant and androgen-insensitive DU145 prostate cancer cells, both tumor suppressors altered gene expression of major 5-lipoxygenase (LOX) and 15-LOXs, including response to T helper 2 (Th2)-cytokine [interleukin-4 (IL-4)] and endogenous steroids (mimicked by dexamethasone). Wild-type and mutant ANXA7 distinctly affected expression of the dexamethasone-induced 15-LOX-2 (a prostate-specific endogenous tumor suppressor) as well as the IL-4-induced 15-LOX-1. On the other hand, wild-type p53 restored 5-LOX expression in DU145 to levels comparable to benign prostate epithelial cells. Using mass spectrometry of DNA affinity-enriched nuclear proteins, we detected different proteins that were bound to adjacent p53 and estrogen response elements in the 5-LOX promoter in DU145 cells introduced with ANXA7 versus p53. Sex hormone regulator 17-B hydroxysteroid dehydrogenase 4 was identified under p53 introduction, which induced the 5-LOX expression. Meantime, nuclear proteins bound to the same 5-LOX promoter site under introduction of ANXA7 (that was associated with the repressed 5-LOX) were identified as zinc finger proteins ZNF433 and Aiolos, pyrin domaincontaining NALP10, and the p53-regulating DNA repair enzyme APEX1. Thus, ANXA7 and p53 can distinctly regulate LOX transcription that is potentially relevant to the AAmediated cell growth control in tumor suppression.

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Section: Cancer Researchmentioning

confidence: 99%

Distinct Effects of Annexin A7 and p53 on Arachidonate Lipoxygenation in Prostate Cancer Cells Involve 5-Lipoxygenase Transcription

et al. 2006

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“…Prostate cancer tissues and cells are equipped with key enzymes of estrogen metabolism, including hydroxylases, whose activity varies according to estrogen receptor status and responsiveness (37). The differences we observed may be related to the disease processes themselves rather than to etiological differences (37)(38)(39)(40).…”

Section: Discussionmentioning

confidence: 86%

Estrogen Metabolism and Prostate Cancer Risk

Muti¹

2001

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“…This evidence is also relevant for other target cells of steroids (Carruba et al, 1997 (Pollow et al, 1977;Strobl and Lippman, 1979;Tait et al, 1989;Poutanen et al, 1993). The oestrogen receptor status is critical for the genesis and/or evolution of a transformed cell phenotype and.…”

Section: Discussionmentioning

confidence: 89%

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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Molecular expression of 17βhydroxysteroid dehydrogenase types in relation to their activity in intact human prostate cancer cells

Cited by 21 publications

References 22 publications

Distinct Effects of Annexin A7 and p53 on Arachidonate Lipoxygenation in Prostate Cancer Cells Involve 5-Lipoxygenase Transcription

Distinct Effects of Annexin A7 and p53 on Arachidonate Lipoxygenation in Prostate Cancer Cells Involve 5-Lipoxygenase Transcription

Estrogen Metabolism and Prostate Cancer Risk

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

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