The N-terminal of the estrogen receptor (ERα) mediates transcriptional cross-talk with the retinoic acid receptor in human breast cancer cells

Rousseau, Caroline; Pettersson, Filippa; Couture, Marie Claude; Paquin, André; Galipeau, Jacques; Mader, Sylvie; Miller, Wilson H.

doi:10.1016/s0960-0760(03)00255-3

Cited by 37 publications

(28 citation statements)

References 69 publications

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“…4B). The induction in MDA-MB-231 cells was reduced, supporting some previous findings (40,46). Furthermore, the transcript levels of established RA target genes RIP140, CRABP2, and HAS2 were induced by RA under estrogen-replete conditions in both MCF-7 and MDA-MB-231 cells (Fig.…”

Section: Ra Inhibits Growth Of Er-positive Breast Cancer Cells and Resupporting

confidence: 90%

“…Retinoids inhibit both the incidence and number of carcinogeninduced mammary tumors in animal models (54 -56). ER-dependent target gene activation is critical to support continued proliferation of ER ϩ breast cancers and several reports suggest that breast cancer growth suppression mediated by retinoids is anti-estrogenic in nature (33,34,36,39,40) with RAR-␣ playing a major role in initiating RA signaling (35,57,58). Data presented in this study further confirm these findings.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have suggested that retinoids predominately inhibit the growth of estrogen-dependent but not hormone refractory breast cancers (31)(32)(33)(34)(35)(36)(37)(38). Although the underlying mechanism remains elusive, there is evidence to suggest that the growth suppressive effects of retinoids may be, in part, anti-estrogenic in nature (33,34,36,39,40). The current study was designed to assess the role of RIP140 as a mechanism of cross-talk between RAR and ER signaling.…”

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confidence: 99%

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Limiting Effects of RIP140 in Estrogen Signaling

White¹,

Yore

Deng

et al. 2005

Journal of Biological Chemistry

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The receptor interacting protein 140 (RIP140) belongs to a unique subclass of nuclear receptor coregulators with the ability to bind and repress the action of a number of agonist-bound hormone receptors. We have previously demonstrated that all-trans-retinoic acid (RA) induction of RIP140 constitutes a rate-limiting step in the regulation of retinoid receptor signaling. Here we demonstrate that RIP140 is also a limiting regulator of estrogen receptor signaling. Overexpression of RIP140 dose dependently inhibits estrogen-dependent reporter activity in human breast cancer cells. Furthermore, small interfering RNA to RIP140 enhances estrogen-dependent signaling. Our previous studies indicate that RIP140 is a direct target of RA. We report here that RA can abrogate estrogen-mediated cell cycle re-entry. In addition, RA treatment of estrogen-dependent breast cancer cells opposes estrogen receptor-dependent reporter activity, implying that a proportion of RA effects are anti-estrogenic. We provide evidence for a role for RIP140 in mediating anti-estrogenic effects of RA. RIP140 small interfering RNA blocks RA-mediated repression of estrogen receptor activity and provides a growth advantage to estrogen-dependent cells. Together these data implicate a regulatory role for RIP140 in mediating anti-estrogenic effects of RA in estrogendependent breast cancer cells and suggest that acute regulation of coregulator expression may be a general mechanism to integrate diverse hormone signals.

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Section: Ra Inhibits Growth Of Er-positive Breast Cancer Cells and Resupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Limiting Effects of RIP140 in Estrogen Signaling

White¹,

Yore

Deng

et al. 2005

Journal of Biological Chemistry

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“…There could be favorable pharmacokinetic and pharmacodynamic interactions of these drugs in tumor cells (Appierto et al, 2001;Aoyama, 2002). There could be a co-operative regulation of the same or distinct cellular targets by these drugs independent of their role in cell cycle progression (Favoni et al, 1998;Brockdorff et al, 2003;Mitsiades et al, 2003;Rousseau et al, 2003). Other possible nonoverlapping mechanisms include the induction of ceramide-directed apoptosis, free radical generation and induction of NOS by these drugs (Maurer et al, 2000;Erdreich-Epstein et al, 2002;Simeone et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Targeting cyclin D1, a downstream effector of INI1/hSNF5, in rhabdoid tumors

et al. 2005

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Rhabdoid tumors (RTs) are aggressive and currently incurable pediatric malignancies. INI1/hSNF5 is a tumor suppressor biallelically inactivated in RTs. Our previous studies have indicated that cyclin D1 is a key downstream target of INI1/hSNF5 and genesis and/or survival of RTs in vivo is critically dependent on the presence of cyclin D1. In this report, we have tested the hypothesis that therapeutic targeting of cyclin D1 is an effective means of treating RTs. We found that RNA interference of cyclin D1 in rhabdoid cells was sufficient to induce G1 arrest and apoptosis. Furthermore, we found that pharmacological intervention with low micromolar concentrations of N-(4-hydroxyphenyl)retinamide (4-HPR), which downmodulates cyclin D1, induced G1 arrest and apoptosis in rhabdoid cell lines. 4-HPR in combination with 4-hydroxy-tamoxifen (4OH-Tam), synergistically inhibited survival as well as anchorage-dependent and -independent growth of rhabdoid cells and caused synergistic induction of cell cycle arrest and apoptosis. 4-HPR and tamoxifen exhibited synergistic growth inhibition of RTs in xenograft models in vivo. The effects of combination of drugs were correlated to the depletion of cyclin D1 levels both in in vitro and in vivo tumor models. These results demonstrate that 4-HPR and tamoxifen are effective chemotherapeutic agents for RTs. We propose that downmodulation of cyclin D1 is a novel and effective therapeutic strategy for RTs.

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“…ERa, RARa and CRABPII genes are coexpressed in human breast cells (Figure 1), suggesting that their expression, two of which are transcription factors, is coordinately regulated. It has been reported that ERa transcriptionally upregulates RARa expression (Roman et al, 1993;van der Leede et al, 1995;Rousseau et al, 2003) and RARa transcriptionally upregulates CRAB-PII expression (Astrom et al, 1992), suggesting a simplest hypothesis that ERa to RARa to CRABPII cascade exists. However, recent reports demonstrated that, in rat uterine cells, estradiol directly upregulates, but ATRA does not, CRABPII transcription (Bucco et al, 1997;Li and Ong, 2003), raising the prospect that ERa may independently regulate RARa and CRABPII expression.…”

Section: Discussionmentioning

confidence: 99%

Expression of estrogen receptor α, retinoic acid receptor α and cellular retinoic acid binding protein II genes is coordinately regulated in human breast cancer cells

et al. 2005

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Human breast cancer cell lines expressing the estrogen receptor a (ERa), all-trans-retinoic acid (ATRA) receptor a (RARa) and cellular retinoic acid binding protein II (CRABPII) genes are sensitive to ATRA-mediated growth inhibition. To study the relationship among ERa, RARa and CRABPII expression, the protein levels of each member were compared in five breast cancer cell lines (T47D, MCF-7, ZR-75-1, Hs587 T and MDA-MB-231 cells) and two immortalized nontumorigenic breast epithelial cell lines (MTSV1.7 and MCF-10A). ERa, RARa and CRABPII proteins were detected in T47D, MCF-7 and ZR-75-1 cells but not in other tested cell lines. RARa and CRABPII proteins were either reduced or undetectable in T47D/C4:2W and MCF-7/ADR cells with lost expression of ERa. Estradiol increased and antiestrogens (tamoxifen and ICI 164,384) downregulated the expression of both RARa and CRABPII proteins in T47D and MCF-7 cells. RARa antagonist Ro-41-5253 inhibited CRABPII expression, but not RARa expression in estradiol-treated T47D and MCF-7 cells. Suppression of ERa by small interfering RNA (siRNA) reduced RARa and CRABPII gene expression and siRNA suppression of RARa reduced CRABPII expression while having no effect on ERa in T47D cells. Transient transfection of either RARa or ERa expression vectors increased CRABPII expression in MDA-MB-231 cells but only RARa, not ERa, activated hCRABPII promoter reporter. These results indicate that there is a gene activation pathway in which ERa drives RARa transcription and RARa drives CRABPII transcription in ERa-positive human breast cancer cells.

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The N-terminal of the estrogen receptor (ERα) mediates transcriptional cross-talk with the retinoic acid receptor in human breast cancer cells

Cited by 37 publications

References 69 publications

Limiting Effects of RIP140 in Estrogen Signaling

Limiting Effects of RIP140 in Estrogen Signaling

Targeting cyclin D1, a downstream effector of INI1/hSNF5, in rhabdoid tumors

Expression of estrogen receptor α, retinoic acid receptor α and cellular retinoic acid binding protein II genes is coordinately regulated in human breast cancer cells

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