Regulation of vascular endothelial growth factor (VEGF) gene transcription by estrogen receptors α and β

Mueller, Michael D.; Vigne, Jean-Louis; Minchenko, О. H.; Lebovic, Dan I.; Leitman, Dale C.; Taylor, Robert N.

doi:10.1073/pnas.200377097

Cited by 322 publications

(234 citation statements)

References 60 publications

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“…ER-b is well known to be implicated in tissue healing secondary to different types of injuries. [16][17][18][19][20] Its expression was found previously to be significantly increased after irradiation of rat mammary gland. 23 Even though ER-b is only upregulated transiently in the soft tissues in fracture healing.…”

Section: Discussionmentioning

confidence: 81%

“…The primer sequences were described previously. 20,21 To perform radioactive PCR, the oligonucleotides were end labeled using 32Pg-ATP. For the first strand complementary DNA synthesis, 1 lg of total RNA was reverse transcribed with Superscript I Reverse Transcriptase (Gibco BRL, Grand Island, NY), using hexamers in a reaction volume of 80 ll.…”

Section: Rt-pcrmentioning

confidence: 99%

“…[17][18][19] The role of ER-a, ER-b and PR in regulating response to vascular injury was shown. 20,21 Most notably, it was postulated that ER-b, via an AP1-like antioxidant response element, may regulate expression of quinone reductase, an enzyme implied in control of reactive oxygen species (ROS) and free radicals. 22 Significantly higher levels of estrogen receptor were documented in breast tissue several months after irradiation in animal experiments.…”

mentioning

confidence: 99%

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Differential expression of steroid receptors in prostate tissues before and after radiation therapy for prostatic adenocarcinoma

Torlakovic

Lilleby²,

Berner

et al. 2005

Intl Journal of Cancer

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The expression, distribution and the role of steroid receptors in benign and malignant untreated prostate tissues is well recognized, however, the status of steroid receptors in prostate after radiotherapy (RT) for adenocarcinoma has not yet been studied fully. Immunohistochemical evaluation of androgen receptor (AR), estrogen receptor-alpha (ER-a), estrogen receptor-beta (ER-b), and progesterone receptor (PR) was carried out in prostate needle biopsies obtained before and after radiotherapy from 60 patients with adenocarcinoma. The ER-b transcripts were also studied by RT-PCR in LNCaP prostate carcinoma cell line before and 24 hr after c-irradiation at 0.5 Gy and 8.0 Gy. Significantly higher level of ER-b expression was found in post-radiation samples of prostate adenocarcinoma and benign epithelium. After RT, all steroid receptors were upregulated in prostatic stroma. Tumor AR expression did not change significantly. Although a positive association between AR and ER-b expression was observed in pretreatment prostate adenocarcinoma, it was lost after RT suggesting that these 2 steroid receptors respond differently to RT. High levels of pretreatment tumor ER-b were associated with local recurrence after RT and decreased biochemical recurrence-free survival (p 5 0.028). LNCaP cell line that expressed no ER-b mRNA before c-irradiation, clearly expressed ER-b mRNA 24 hr after 0.5 Gy and 8.0 Gy. Upregulation of all steroid receptors in the prostate stroma and upregulation of ER-b in the tumor epithelium after RT, may represent a protective tissue response to radiation-induced tissue injury. Although stromal AR was doubled after RT, the tumor and benign epithelium expression of AR seemed resistant to change by RT. ' 2005 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 81%

Section: Rt-pcrmentioning

confidence: 99%

mentioning

confidence: 99%

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Differential expression of steroid receptors in prostate tissues before and after radiation therapy for prostatic adenocarcinoma

Torlakovic

Lilleby²,

Berner

et al. 2005

Intl Journal of Cancer

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“…The same element on the VEGF promoter was previously shown to bind ERa and to exhibit E 2 responsiveness (Buteau-Lozano et al 2002). Several estrogen-responsive regions were located on the VEGF promoter; however, only few were found to be functionally active (Hyder et al 2000, Mueller et al 2000. Alternatively, ERa and c-Myc may interact with SP proteins through binding to GC-rich motif on the VEGF promoter (K66 to K47) as was shown in ZR-75-1 cells (Stoner et al 2004).…”

Section: Discussionmentioning

confidence: 99%

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

Dadiani¹,

Seger²,

Kreizman³

et al. 2009

Endocrine-Related Cancer

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The role of c-Myc in estrogen regulation of vascular endothelial growth factor (VEGF) and of the vasculature function has been investigated in breast cancer cells and tumors. The studies were performed on MCF7 wild-type cells and MCF7-35im clone, stably transfected with an inducible c-Myc gene. In vitro and ex vivo methods for investigating molecular events were integrated with in vivo magnetic resonance imaging of the vascular function. The results showed that the c-Myc upregulation by estrogen is necessary for the transient induction of VEGF transcription; however, overexpression of c-Myc alone is not sufficient for this induction. Furthermore, both c-Myc and the activated estrogen receptor a (ERa) were shown to co-bind the VEGF promoter in close proximity, indicating a novel mechanism for estrogen regulation of VEGF. Studies of long-term estrogen treatment and overexpression of c-Myc alone demonstrated regulation of stable VEGF expression levels in vitro and in vivo, maintaining steady vascular permeability in tumors. However, withdrawal of estrogen from the tumors resulted in increased VEGF and elevated vascular permeability, presumably due to hypoxic conditions that were found to dominate VEGF overexpression in cultured cells. This work revealed a cooperative role for ERa and c-Myc in estrogen regulation of VEGF and the ability of c-Myc to partially mimic estrogen regulation of angiogenesis. It also illuminated the differences in estrogen regulation of VEGF during transient and long-term sustained treatments and under different microenvironmental conditions, providing a complementary picture of the in vitro and in vivo results.

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“…Although hormone responsive (105)(106)(107)(108), the VEGF promoter lacks canonical AR or estrogen receptor (ER)-binding sites. VEGF regulation by estrogen in endometrial and breast cancer cells involves interactions of ER-α and Sp1 (or Sp3) with GC boxes in the core promoter region of VEGF (-66 to -47 bases from start site) (108,109).…”

Section: Combined Androgen and Wt1 Activation Of Vegf Expression In Hmentioning

confidence: 99%

Functional Role of WT1 in Prostate Cancer

et al. 2016

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Licence: This open access article is licensed under Creative Commons Attribution 4.0 International (CC BY 4.0). http://creativecommons.org/licenses/by/4.0/ Users are allowed to share (copy and redistribute the material in any medium or format) and adapt (remix, transform, and build upon the material for any purpose, even commercially), as long as the authors and the publisher are explicitly identified and properly acknowledged as the original source. AbstractAlthough initial discoveries of Wilms tumor 1 (WT1) expression in extrarenal disease generated controversy, we and others have examined WT1 expression in non-Wilms cancers and have demonstrated that the WT1(A) isoform, lacking the lysine-threonine-serine tripeptide (KTS) insertion, transcriptionally regulates the expression of growth control genes in other cancer types. Here, we review our evidence that WT1 is expressed in prostate cancer (PC) epithelial cells and regulates PC critical genes. That WT1 may promote metastatic disease is consistent with previous findings that WT1 suppressed E-cadherin and enhanced motility of PC cells with low migratory and metastatic potential. Recent findings led us to askFraizer et al. 236whether WT1 acts as an angiogenic switch in PC. Although vascular endothelial growth factor (VEGF) is regulated at several levels and by a number of different factors, a mechanistic understanding of WT1-mediated transcriptional regulation in PC cells was previously lacking. Here, we discuss the evidence of WT1-and androgen receptor (AR)-binding sites in the VEGF promoter and show the potential for cooperation between hormone and WT1. These findings revealed that in AR-intact PC cells, WT1 was sufficient to upregulate VEGF transcription, and WT1 expression enhanced the hormone activation of VEGF expression. This notion that WT1 can activate an angiogenic switch in PC cells, to enhance tumor growth and progression to metastatic disease, is consistent with our understanding of the oncogenic nature of WT1 overexpression in inappropriate tissues or at inappropriate times. The potential for WT1 to promote both tumor angiogenesis and PC cell migration suggests that WT1 regulates genes that promote PC progression to lethal metastatic disease. Therapies targeting WT1 in PC may reduce metastatic spread and increase overall survival.

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Regulation of vascular endothelial growth factor (VEGF) gene transcription by estrogen receptors α and β

Cited by 322 publications

References 60 publications

Differential expression of steroid receptors in prostate tissues before and after radiation therapy for prostatic adenocarcinoma

Differential expression of steroid receptors in prostate tissues before and after radiation therapy for prostatic adenocarcinoma

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

Functional Role of WT1 in Prostate Cancer

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