Estrogen regulation of vascular endothelial growth factor in breast cancer in vitro and in vivo: the role of estrogen receptor α and c-Myc

Dadiani, Maya; Seger, Dalia; Kreizman, Tamar; Badikhi, Daria; Margalit, Raanan; Eilam, Raya; Degani, Hadassa

doi:10.1677/erc-08-0249

Cited by 39 publications

(33 citation statements)

References 46 publications

(52 reference statements)

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“…Interestingly, recent studies have identified pro-and anti-angiogenic VEGF splice forms (Bates et al 2002), which are differentially regulated in cancers, including in PCa (Woolard et al 2004, Mavrou et al 2014, and which (A) The VEGF promoter is regulated by a diverse array of transcription factors, hypoxia-inducible factors (HIFs), specificity protein-1 (Sp1), and most notably in the context of the present review, multiple nuclear receptors, including androgen (Eisermann et al 2013) and estrogen (Buteau-Lozano et al 2002, Dadiani et al 2009), which are indicated in red and yellow respectively. In addition, the VEGF promoter is regulated by progesterone (Wu et al 2004), vitamin D (Cardus et al 2009), and the liver-X nuclear receptors (LXR) (Walczak et al 2004).…”

Section: Transcriptional Regulation Of Pro-angiogenesis Pathways In Pcamentioning

confidence: 89%

“…However, over the past decade, it has become apparent that the VEGF promoter can be regulated by multiple members of the nuclear receptor family, including the AR (Eisermann et al 2013), estrogen (ERa/cMyc) (ButeauLozano et al 2002, Dadiani et al 2009), progesterone (Wu et al 2004), vitamin D (Cardus et al 2009, and the liver-X receptors (Walczak et al 2004). Consistent with this, animal studies have indicated a role for androgens and estrogen in prostate vascularization (Daehlin et al 1985).…”

Section: Transcriptional Regulation Of Pro-angiogenesis Pathways In Pcamentioning

confidence: 98%

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Regulation of vascular endothelial growth factor in prostate cancer

Brot¹,

Ntekim²,

Cardenas³

et al. 2015

Endocrine-Related Cancer

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Prostate cancer (PCa) is the most common malignancy affecting men in the western world. Although radical prostatectomy and radiation therapy can successfully treat PCa in the majority of patients, up to w30% will experience local recurrence or metastatic disease. Prostate carcinogenesis and progression is typically an androgen-dependent process. For this reason, therapies for recurrent PCa target androgen biosynthesis and androgen receptor function. Such androgen deprivation therapies (ADT) are effective initially, but the duration of response is typically %24 months. Although ADT and taxane-based chemotherapy have delivered survival benefits, metastatic PCa remains incurable. Therefore, it is essential to establish the cellular and molecular mechanisms that enable localized PCas to invade and disseminate. It has long been accepted that metastases require angiogenesis. In the present review, we examine the essential role for angiogenesis in PCa metastases, and we focus in particular on the current understanding of the regulation of vascular endothelial growth factor (VEGF) in localized and metastatic PCa. We highlight recent advances in understanding the role of VEGF in regulating the interaction of cancer cells with tumor-associated immune cells during the metastatic process of PCa. We summarize the established mechanisms of transcriptional and post-transcriptional regulation of VEGF in PCa cells and outline the molecular insights obtained from preclinical animal models of PCa. Finally, we summarize the current state of anti-angiogenesis therapies for PCa and consider how existing therapies impact VEGF signaling.

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Section: Transcriptional Regulation Of Pro-angiogenesis Pathways In Pcamentioning

confidence: 89%

Section: Transcriptional Regulation Of Pro-angiogenesis Pathways In Pcamentioning

confidence: 98%

Regulation of vascular endothelial growth factor in prostate cancer

Brot¹,

Ntekim²,

Cardenas³

et al. 2015

Endocrine-Related Cancer

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“…Previous studies recognized estrogen and testosterone as angiogenic mediators (6)(7)(8)(9). Estrogens enhance angiogenesis by promoting cell attachment, migration, proliferation, and differentiation (10).…”

Section: Introductionmentioning

confidence: 99%

Gnagliosides and Sex Hormones in Human Melanoma

Nicolae¹

2011

Acta Endo (Buc)

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Background. Malignant melanoma is the most aggressive form of skin cancer with a rapidly increasing incidence rate. In contrast to other tumors, the role of sex steroid hormones in the initiation and progression of melanoma remains unclear.Objective. To assess the interaction between the content and composition of gangliosides and sex steroid hormones 17βestradiol (E2) and testosterone (T) in malignant melanoma.Patients and methods. The analysis included 45 melanoma patients (age 28-86; 14 men, 15 non -pregnant women in mid follicular phase and 16 postmenopausal women) and 46 healthy controls. Serum levels of gangliosides (GM1-3, GD1 a,b ,2,3, GT1b, GQ1b), estradiol, testosterone measured in serum by chromatographic and immunochemiluminescence methods were correlated with sex and age.Results. Steroid hormones levels showed no differences between groups (p>0.05), while total gangliosides in normal serum were significantly lower than total ganglioside concentrations determined in melanoma samples (18.63 ± 3.17 mg/dL versus 74.82 ± 34.56 mg/dL) (p<0.05). There were no differences related to sex or age within groups regarding total gangliosides levels. Gangliosides pattern in melanoma patients compared to control showed lower GM3, higher GD3, lower GM3/GD3 ratio, increased GD2 levels, and no significant variation of GM1, GM2, GD1a, GT1b gangliosides. There is a positive correlation between estradiol levels and total gangliosides concentration both in non-pregnant premenopausal and postmenopausal melanoma patients. GM3 is negatively correlated with estradiol levels in melanoma group, GT1b and O-Acetyl GD3 concentrations are positively correlated with estradiol levels in women with melanoma. Testosterone levels showed no significant correlation with the content and pattern of gangliosides in melanoma patients.Conclusions. The correlations between content and composition of gangliosides and estradiol in melanoma suggest a possible role of these molecules in melanoma behavior.

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“…In breast cancer cell lines MDA-MB-231 and T47D, which express only ERβ, previous data showed that VEGF levels were unchanged after treatment with E2. The heterodimerisation of ERα/ERβ may inhibit oestrogen-induced VEGF expression (Dadiani et al 2009), which may explain the lack of E2 response in OVCAR-3 cells containing both ERα/ ERβ.…”

Section: Discussionmentioning

confidence: 99%

Effects of bisphenol A and 17β-estradiol on vascular endothelial growth factor A and its receptor expression in the non-cancer and cancer ovarian cell lines

Ptak

Gregoraszczuk

2015

Cell Biol Toxicol

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Tumours secrete several pro-angiogenic factors, among which vascular endothelial growth factor (VEGF) and its receptor (VEGF-R) are the most extensively studied but not in ovarian cancer cells. The study was designed to investigate the effect of bisphenol A (BPA) (environmental oestrogen) and of 17β-estradiol (E2) (endogenous estrogen) on the gene (real-time PCR) and protein (Western blotting) expression of VEGF-R2 and VEGF-A in human non-cancer (HOSEpiC) and ovarian cancer cell lines (SKOV-3 and OVCAR-3). In addition, VEGF-A levels were measured in culture supernatants using a colorimetric assay. Cells were exposed to BPA (1, 40 and 100 nM) or 17β-estradiol (0.1, 10 and 40 nM) for 3 to 48 h. Since differential expression levels of basal oestrogen receptor (ERα and ERβ) between non-cancer and cancer cell lines may affect the response to oestrogens, receptor expression was measured both at the gene and protein levels. Basal ERβ expression was similar in all cell lines, and ERα expression was significantly higher in the SKOV-3 cell line. Basal VEGF-R2 expression was higher in cancer than non-cancer cell lines, and in contrast, VEGF-A expression was significantly lower in both SKOV-3 and OVCAR-3 cancer cell lines. Exposure of non-cancer cells to BPA and E2 was associated with a significant increase in VEGF-R2 expression but had no effect on VEGF-A expression or secretion. In contrast, exposure of cancer cells to BPA, but not E2, increased VEGF-R2 and VEGF-A expression and secretion. In conclusion, (1) BPA and E2 regulated VEGF-R2 and VEGF-A expression differently in non-cancer and cancer cells, and (2) BPA has a direct stimulatory effect on VEGF-R2 and VEGF-A expression in both, while E2 appears to be uninvolved in the regulation of VEGF-R2 and VEGF-A expression in cancer cells. Graphical Abstract A schematic representation showing BPA and E2 action on VEGF-R2 and VEGF-A expression in non-cancer (HOSEpiC) and cancer cells (SKOV-3, OVCAR-3).

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Estrogen regulation of vascular endothelial growth factor in breast cancer in vitro and in vivo: the role of estrogen receptor α and c-Myc

Cited by 39 publications

References 46 publications

Regulation of vascular endothelial growth factor in prostate cancer

Regulation of vascular endothelial growth factor in prostate cancer

Gnagliosides and Sex Hormones in Human Melanoma

Effects of bisphenol A and 17β-estradiol on vascular endothelial growth factor A and its receptor expression in the non-cancer and cancer ovarian cell lines

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