Binding Interactions between Long Noncoding RNA HOTAIR and PRC2 Proteins

Wu, Liang; Murat, Pierre; Matak-Vinković, Dijana; Murrell, Adele; Balasubramanian, Shankar

doi:10.1021/bi401085h

Cited by 161 publications

(165 citation statements)

References 29 publications

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“…Admittedly, quantitative binding experiments of PRC2 to RNA are technically challenging, given that PRC2 is a large multiprotein subunit complex, of up to 640 kDa in its dimeric state (Davidovich et al 2014). Moreover, some of the minimal RNA sequence elements that were previously suggested to be required for PRC2 binding are large, in the range of 80-500 nt (Tsai et al 2010;Klattenhoff et al 2013;Wu et al 2013;Cifuentes-Rojas et al 2014).…”

Section: Promiscuous Rna Binding By Prc2mentioning

confidence: 99%

The recruitment of chromatin modifiers by long noncoding RNAs: lessons from PRC2

Davidovich

Cech

2015

RNA

259

224

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Polycomb repressive complex-2 (PRC2) is a histone methyltransferase required for epigenetic silencing during development and cancer. Among chromatin modifying factors shown to be recruited and regulated by long noncoding RNAs (lncRNAs), PRC2 is one of the most studied. Mammalian PRC2 binds thousands of RNAs in vivo, and it is becoming a model system for the recruitment of chromatin modifying factors by RNA. Yet, well-defined PRC2-binding motifs within target RNAs have been elusive. From the protein side, PRC2 RNA-binding subunits contain no known RNA-binding domains, complicating functional studies. Here we provide a critical review of existing models for the recruitment of PRC2 to chromatin by RNAs. This discussion may also serve researchers who are studying the recruitment of other chromatin modifiers by lncRNAs.

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Section: Promiscuous Rna Binding By Prc2mentioning

confidence: 99%

The recruitment of chromatin modifiers by long noncoding RNAs: lessons from PRC2

Davidovich

Cech

2015

RNA

259

224

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“…81 HOTAIR recruits PRC2 to specific target genes, leading to H3K27 trimethylation and epigenetic silencing of metastatic suppressor genes. 82 Further mechanistic investigation into the regulation of metastasis by HOTAIR is necessary. In breast cancer cells, HOTAIR may indirectly increase expression of STAT3.…”

Section: Hox Transcript Antisense Rna (Hotair)mentioning

confidence: 99%

Epigenetic regulation in human melanoma: past and future

Sarkar

Leung

Baguley³

et al. 2015

Epigenetics

243

174

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“…HOTAIR is derived from HOX C, but functions in trans at the HOX D locus (65). HOTAIR recruits the PRC2 complex and the demethylase LSD1, promoting an increase in the repression code H3K27me3 and a decrease in the activation code H3K4me3 (66,67). In addition to these functions, in lung cancer, HOTAIR has been identified as a scaffold to facilitate the binding of E3 ubiquitinylases and corresponding substrates Ataxin-1 and Snurportin ( Figure 1C) (68).…”

Section: Hox Antisense Intergenic Rna (Hotair)mentioning

confidence: 99%

Long Non-coding RNAs and their Role in Metastasis

Weidle

Birzele

Kollmorgen

et al. 2017

CGP

168

124

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Abstract.Metastasis is the major cause of death in patients with cancer. It is mediated by a multi-step process referred to as the metastatic cascade (1, 2). Initial steps include local invasion and migration, angiogenesis, epithelialmesenchymal transition (EMT) and intravasation. Tumor cells enter the circulation as single cells or circulating tumor cell clusters, are coated by platelets to escape an immune response and subsequently arrest in capillaries in distant organs as a prerequisite for extravasation. Colonization starts by homing of tumor cells in supporting niches of the organ parenchyma, followed by a latency phase which can last from several months to decades. A prerequiste for overt outgrowth of micrometastases is their adaptation to the local microenvironment and acquisition of colonisation-promoting traits (3-6). The pattern of colonized distant organs depends on the tumor type and can range from predominant spread to one organ and colonization of different types of organs sequentially or simultaneously (7). Several genes and their products have been identified to mediate crucial steps of the metastatic process such as metastasis initiation and progression, as well as organ-specific functions of metastasis (virulence) (8, 9). These gene products include proteases, chemokines, cytokines and their receptors, angiogenic factors, intracellular and transmembrane kinases, adhesion molecules, components of the extracellular matrix (ECM), GPI-linked receptors and carbohydrate metabolism-related enzymes (8, 9). More recently, an important impact of RNA-related molecules for metastasis has emerged. MicroRNAs (miRs) and other types of RNA modulate metastasis via regulatory networks (10,11). In this review we focus on the role of long non-coding RNAs (lncRNA) as promoters or inhibitors of metastasis in different tumor entities since there is an urgent need to define new targets for therapeutic intervention. With the exception of denosumab for treatment of bone metastases, all other agents evaluated in clinical studies for treatment of metastatic disease gave rise to mixed or disappointing results (6).

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Binding Interactions between Long Noncoding RNA HOTAIR and PRC2 Proteins

Cited by 161 publications

References 29 publications

The recruitment of chromatin modifiers by long noncoding RNAs: lessons from PRC2

The recruitment of chromatin modifiers by long noncoding RNAs: lessons from PRC2

Epigenetic regulation in human melanoma: past and future

Long Non-coding RNAs and their Role in Metastasis

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