Cross-talk between Transforming Growth Factor-β and Estrogen Receptor Signaling through Smad3

Matsuda, Tadashi; Yamamoto, T.; Muraguchi, Atsushi; Saatcioglu, Fahri

doi:10.1074/jbc.m105316200

Cited by 235 publications

(211 citation statements)

References 41 publications

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“…Three (ER-a, ER-b and AR) of 4 steroid receptors, which we found in the current study to have higher expression after RT, were found previously to have an ability to inactivate TGF-b antiproliferative signaling pathway by inhibition of Smad3. [35][36][37][38][39] Interestingly, ER-b was the only steroid receptor to be upregulated in prostate adenocarcinoma epithelial cells after RT. We have demonstrated previously that ER-b expression is associated positively with Gleason score and primary Gleason grade with higher levels expressed in higher grade tumors.…”

Section: Discussionmentioning

confidence: 99%

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: 99%

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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“…and Western blotting were performed as previously described [21]. The cells were harvested and lysed in lysis buffer (50 mM Tris-HCl, pH 7.4, 0.15 M NaCl, 1% NP-40, 1 mM sodium orthovanadate, 1 mM phenylmethylsulfonyl fluoride, and 10 mg /ml each of aprotinin, pepstatin, and leupeptin).…”

Section: Immunoprecipitation Immunoblotting and Dna Binding Assay Imentioning

confidence: 99%

Epstein–Barr virus-derived EBNA2 regulates STAT3 activation

Muromoto

Ikeda

Okabe

et al. 2009

Biochemical and Biophysical Research Communications

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The Epstein-Barr virus (EBV)-encoded latency protein EBNA2 is a nuclear transcriptional activator that is essential for EBV-induced cellular transformation. Here, we show that EBNA2 interacts with STAT3, a signal transducer for an interleukin-6 family cytokine, and enhances the transcriptional activity of STAT3 by influencing its DNA-binding activity. Furthermore, EBNA2 cooperatively acts on STAT3 activation with LMP1. These data demonstrate that EBNA2 acts as a transcriptional coactivator of STAT3.3

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“…Another group detected an in vitro binding of immobilized c-jun to recombinant ERa, simultaneously negating an interaction of ERa and c-fos [31]. Moreover, Matsuda et al [32] demonstrated that ERa suppresses TGF-b signaling in the presence of estrogen by complex formation with Smad3, and Wu et al [33] showed an ERa-Smad4 interaction. Nevertheless, there are some reports dealing with a repressor or co-repressor function of ERa on specific DNA sequences.…”

Section: Discussionmentioning

confidence: 99%

Estrogen receptor α attenuates transforming growth factor-β signaling in breast cancer cells independent from agonistic and antagonistic ligands

Stope

Popp²,

Knabbe³

et al. 2009

Breast Cancer Res Treat

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To investigate a presumed crosstalk between estrogen receptor a (ERa) and the TGF-b signaling pathway in breast cancer, we analyzed the TGF-b-induced expression of the plasminogen activator inhibitor 1 (PAI-1) gene in ER-positive MCF-7 cells. After siRNA-mediated knock-down of endogenous ERa, the transcription level of PAI-1 was upregulated, pointing to an attenuation of TGF-b signaling by the presence of ERa. We verified these findings by a vice versa approach using a primary ER-negative cell model transiently overexpressing either ERa or ERb. We found that ERa, but not ERb, led to a strong inhibition of the TGF-b1 signal, monitored by TGF-b reporter assays. This attenuation was completely independent of receptor stimulation by b-estradiol (E2) or inhibition by the pure antagonist ICI 182.780 (ICI). Our results indicate a permanent repression of PAI-1 by ERa and suggest a ligand-independent crosstalk between ERa and TGF-b signaling in breast cancer cells.

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Cross-talk between Transforming Growth Factor-β and Estrogen Receptor Signaling through Smad3

Abstract: Transforming growth factor-␤ (TGF-␤

Cited by 235 publications

References 41 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

Epstein–Barr virus-derived EBNA2 regulates STAT3 activation

Estrogen receptor α attenuates transforming growth factor-β signaling in breast cancer cells independent from agonistic and antagonistic ligands

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