Aberrant expression of SWI/SNF catalytic subunits BRG1/BRM is associated with tumor development and increased invasiveness in prostate cancers

Sun, Aihua; Tawfik, Ossama; Gayed, Bishoy A.; Thrasher, J. Brantley; Hoestje, Sara M; Li, Chaoyang; Li, Benyi

doi:10.1002/pros.20521

Cited by 120 publications

(97 citation statements)

References 44 publications

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“…In fact, BRG1 may act in an oncogenic manner in some tumors (Wang et al, 2009). Furthermore, increased expression of BRG1 has been associated with tumor growth and invasiveness in prostate tumors (Sun et al, 2007) as well as higher metastatic behavior in gastric carcinomas (Sentani et al, 2001). Although brg1 heterozygotes have higher incidence of tumors, it is worth noting that these are mostly differentiated epithelial tumors (Bultman et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Although loss of BRG1 and/or BRM-the two mutually exclusive ATPase subunits of the SWI/SNF chromatin-remodeling complex-is found in a number of cancer lines and primary tumors (Reisman et al, 2009), expression of BRG1, but not of BRM, has also been correlated with higher invasive/metastatic behavior in carcinomas (Sentani et al, 2001;Sun et al, 2007). BRG1 associates with DNA-binding transcription factors and histone-modifying enzymes to activate/repress transcription as well as to regulate DNA replication, repair and recombination (Trotter and Archer, 2008).…”

Section: Introductionmentioning

confidence: 99%

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ZEB1 represses E-cadherin and induces an EMT by recruiting the SWI/SNF chromatin-remodeling protein BRG1

et al. 2010

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Loss of E-cadherin is a key initial step in the transdifferentiation of epithelial cells to a mesenchymal phenotype, which occurs when tumor epithelial cells invade into surrounding tissues. Expression of the nuclear factor ZEB1 induces an epithelial-to-mesenchymal transition and confers a metastatic phenotype on carcinomas by repressing the E-cadherin gene at the transcriptional level.In this study, we show that ZEB1 interacts with the SWI/ SNF chromatin-remodeling protein BRG1 to regulate E-cadherin independently of CtBP, its traditional corepressor. Blocking the interaction between ZEB1 and BRG1 induces expression of E-cadherin and downregulation of the mesenchymal marker vimentin. ZEB1 and BRG1 colocalize in E-cadherin-negative cells from cancer lines and in the stroma of normal colon. Colocalization of ZEB1 and BRG1 in epithelial cells is only found in those de-differentiated cells characterized by nuclear b-catenin staining at the invasive edge of the tumor. Our results identify ZEB1/BRG1 as a new transcriptional mechanism regulating E-cadherin expression and epithelial-to-mesenchymal transdifferentiation that may be involved during the initial stages of tumor invasion.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

ZEB1 represses E-cadherin and induces an EMT by recruiting the SWI/SNF chromatin-remodeling protein BRG1

et al. 2010

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“…Nevertheless, our data in metastatic prostate cancer cell line PC3 suggests a possible dependency of select cancers on GLTSCR1 and/or BICRAL. Intriguingly, prostate cancers have BRG1 upregulation, but not SNF5, and display dependencies on BRG1 (40). In addition to prostate cancer, many other cancers display increased dependency on BRG1, although the associated SWI/SNF subcomplex involved in this dependency is unexplored.…”

Section: Proteomic Analysis Of Brg1 Immunoprecipitationsmentioning

confidence: 99%

Glioma tumor suppressor candidate region gene 1 (GLTSCR1) and its paralog GLTSCR1-like form SWI/SNF chromatin remodeling subcomplexes

Alpsoy

Dykhuizen

2018

Journal of Biological Chemistry

170

154

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“…2) including nucleoplasmin 2, basonuclin, the transcription intermediate factor 1 (Tif1) and the chromatin factor Brg1 (Minami et al, 2007;Sun et al, 2007;Torres-Padilla et al, 2006;Zernicka-Goetz et al, 2009). Nucleoplasmin 2 is required for protamine exchange and basonuclin stimulates RNPI and II transcription.…”

Section: Reprogramming and Preimplantation Development (Pid)mentioning

confidence: 99%

Natural and artificial routes to pluripotency

Krueger¹,

Swanson²,

Tanasijevic³

et al. 2010

Int. J. Dev. Biol.

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Pluripotent cells of the blastocyst inner cell mass (ICM) and their in vitro derivatives, embryonic stem (ES) cells, contain genomes in an epigenetic state that are poised for subsequent differentiation. Their chromatin is hyperdynamic in nature and relatively uncondensed. In addition, a large number of genes are expressed at low levels in both ICM and ES cells. Also, the chromatin of naturally pluripotent cells contains specialized histone modification patterns such as bivalent domains, which mark genes destined for later developmentally-regulated expression states. Female pluripotent cells contain X chromosomes that have yet to undergo the process of X chromosome inactivation. Collectively, these features of very early embyronic chromatin are required for the successful specification and production of differentiated cell lineages. Artificial reprogramming methods such as somatic nuclear transfer (SCNT), ES cell fusion-mediated reprogramming (FMR), and induced pluripotency (iPS) yield pluripotent cells that recapitulate many features of naturally pluripotent cells, including many of their epigenetic features. However, the route to pluripotent epigenomic states in artificial pluripotent cells differs drastically from that of their natural counterparts. Here, we compare and contrast the differing routes to pluripotency under natural and artificial conditions. In addition, we discuss the intrinsically metastable nature of the pluripotent epigenome and consider epigenetic aspects of reprogramming that may lead to incomplete or inaccurate reprogrammed states. Artificial methods of reprogramming hold immense promise for the development of autologous cell graft sources and for the development of cell culture models for human genetic disorders. However, the utility of artificially reprogrammed cells is highly dependent on the fidelity of the reprogramming process and it is therefore critically important to assess the epigenetic similarities between embryonic and induced pluripotent stem cells.

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Aberrant expression of SWI/SNF catalytic subunits BRG1/BRM is associated with tumor development and increased invasiveness in prostate cancers

Abstract: We provide the first evidence that aberrant expression of BRG1 and BRM genes is associated with disease development and progression in prostate cancers and increased BRG1 expression may promote tumor growth and invasion.

Cited by 120 publications

References 44 publications

ZEB1 represses E-cadherin and induces an EMT by recruiting the SWI/SNF chromatin-remodeling protein BRG1

ZEB1 represses E-cadherin and induces an EMT by recruiting the SWI/SNF chromatin-remodeling protein BRG1

Glioma tumor suppressor candidate region gene 1 (GLTSCR1) and its paralog GLTSCR1-like form SWI/SNF chromatin remodeling subcomplexes

Natural and artificial routes to pluripotency

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