BRG1/BRM and prohibitin are required for growth suppression by estrogen antagonists

Wang, Sheng; Zhang, Baohua; Faller, Douglas V.

doi:10.1038/sj.emboj.7600231

Cited by 59 publications

(80 citation statements)

References 28 publications

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“…12 The frequency with which BRG-1 is inactivated in tumor cell lines including breast cancer, led to studies examining the mechanisms by which BRG-1 inhibits breast cancer epithelial cell proliferation. 5 BRG-1, with prohibitin, blocked MCF-7 cell colony formation and E2F activity 13 providing further evidence that BRG-1 may function as a mammary epithelial cell tumor suppressor.…”

Section: Introductionmentioning

confidence: 80%

Inhibition of cyclin D1 gene transcription by Brg-1

Rao¹,

Casimiro²,

Lisanti³

et al. 2008

Cell Cycle

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The evolutionarily conserved SWI-SNF chromatin remodeling complex regulates cellular proliferation. A catalytic subunit, BRG-1, is frequently down regulated, silenced or mutated in malignant cells, however, the mechanism by which BRG-1 may function as a tumor suppressor or block breast cancer cellular proliferation is not understood. The cyclin D1 gene is a collaborative oncogene overexpressed in greater than 50% of human breast cancers. Herein, BRG-1 inhibited DNA synthesis and cyclin D1 expression in human MCF-7 breast cancer epithelial cells. The cyclin D1 promoter AP-1 and CRE sites were required for repression by BRG-1 in promoter assays. BRG-1 deficient cells abolished and siRNA to BRG-1 reduced, formation of the BRG-1 chromatin complex. The endogenous cyclin D1 promoter AP-1 site bound BRG-1. Estradiol treatment of MCF-7 cells induced recruitment of BRG-1 to the endogenous hpS2 gene promoter. Estradiol, which induced cyclin D1 abundance, was associated with a reduction in recruitment of the co-repressors HP1α/HDAC1 to the endogenous cyclin D1 promoter AP-1/BRG-1 binding sites. These studies suggest the endogenous cyclin D1 promoter BRG-1 binding site functions as a molecular scaffold in the context of local chromatin upon which coactivators and corepressors are recruited to regulate cyclin D1.

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Section: Introductionmentioning

confidence: 80%

Inhibition of cyclin D1 gene transcription by Brg-1

Rao¹,

Casimiro²,

Lisanti³

et al. 2008

Cell Cycle

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show abstract

“…Furthermore, in other cell types, PHB2 has also been suggested to be localized in the nucleus and modulate transcriptional activity by interacting with transcription factors, including nuclear receptors, either directly or indirectly 12,[29][30][31][32] . PHB2 has been shown to interact with and inhibit the transcriptional activity of the ER in breast cancer 12 .…”

Section: Discussionmentioning

confidence: 99%

CARL lncRNA inhibits anoxia-induced mitochondrial fission and apoptosis in cardiomyocytes by impairing miR-539-dependent PHB2 downregulation

et al. 2014

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Abnormal mitochondrial fission participates in the pathogenesis of many diseases. Long non-coding RNAs (lncRNAs) are emerging as new players in gene regulation, but how lncRNAs operate in the regulation of mitochondrial network is unclear. Here we report that a lncRNA, named cardiac apoptosis-related lncRNA (CARL), can suppress mitochondrial fission and apoptosis by targeting miR-539 and PHB2. The results show that PHB2 is able to inhibit mitochondrial fission and apoptosis. miR-539 is responsible for the dysfunction of PHB2 and regulates mitochondrial fission and apoptosis by targeting PHB2. Further, we show that CARL can act as an endogenous miR-539 sponge that regulates PHB2 expression, mitochondrial fission and apoptosis. Our present study reveals a model of mitochondrial fission regulation that is composed of CARL, miR-539 and PHB2. Modulation of their levels may provide a new approach for tackling apoptosis and myocardial infarction.

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“…Alteration of nucleosome structure by ATP-dependent remodeling complexes is a critical step in transcriptional regulation (Muchardt and Yaniv, 1993;Dunaief et al, 1994;Peterson and Tamkun, 1995;Goodwin, 1997;Muchardt et al, 1998;DeCristofaro et al, 1999;Murphy et al, 1999;Yaniv, 1999, 2001;Dahiya et al, 2000;de la Serna et al, 2001;Betz et al, 2002;Reisman et al, 2002;Roy et al, 2002;Wang et al, 2002bWang et al, , 2004Dasgupta et al, 2004;Roche et al, 2004;Inayoshi et al, 2006). The molecular mechanism responsible for these divergent functions of the SWI/ SNF complex has not been fully defined.…”

Section: Introductionmentioning

confidence: 99%

Reprogramming of the SWI/SNF complex for co-activation or co-repression in prohibitin-mediated estrogen receptor regulation

et al. 2007

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The SWI/SNF complex participates as a co-activator in the transcriptional regulation of certain genes. Conversely, we and others have recently established that Brg1 and Brm, the central components of SWI/SNF, act instead as co-repressors for E2F-mediated transcriptional repression, and for the transcription of certain other promoters. We report here that Brg-1 and Brm can switch their mode of function at same promoter between activation and repression by ligand-directed differential coordination with BAF155, BAF170, HDAC1, p300 and prohibitin. This ligand and context-dependent reprogramming of the SWI/SNF complex allows it to differentially serve as either a co-repressor or a co-activator of transcription at the same promoter.

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BRG1/BRM and prohibitin are required for growth suppression by estrogen antagonists

Cited by 59 publications

References 28 publications

Inhibition of cyclin D1 gene transcription by Brg-1

Inhibition of cyclin D1 gene transcription by Brg-1

CARL lncRNA inhibits anoxia-induced mitochondrial fission and apoptosis in cardiomyocytes by impairing miR-539-dependent PHB2 downregulation

Reprogramming of the SWI/SNF complex for co-activation or co-repression in prohibitin-mediated estrogen receptor regulation

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