Identification of p100 target promoters by chromatin immunoprecipitation-guided ligation and selection (ChIP-GLAS)

Liu, Xin; Dong, Lijie; Zhang, Xuejun; Wang, Baoya; Wang, Xinting; Li, Hu; He, Jian‐Qing; Ge, Lin; Xiang, Jing; Yao, Zhi; Yang, Jie

doi:10.1038/cmi.2010.47

Cited by 13 publications

(13 citation statements)

References 12 publications

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“…It was also reported that SND1 could interact with astrocyte elevated gene-1 (AEG-1) in breast cancer and strongly promote lung metastasis (12). In our earlier work using chromatin immunoprecipitation guided ligation and selection (ChIP-GLAS) assays, we have demonstrated that SND1 is potentially involved in the TGFb signaling pathway in breast cancer cells (13). However, it remains unclear how SND1 is upregulated in breast cancer and how SND1 participates in breast cancer metastasis.…”

Section: Introductionmentioning

confidence: 99%

SND1 Acts Downstream of TGFβ1 and Upstream of Smurf1 to Promote Breast Cancer Metastasis

Liu

Cui

et al. 2015

Cancer Research

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SND1 is an AEG-1/MTDH/LYRIC-binding protein that is upregulated in numerous human cancers, where it has been assigned multiple functional roles. In this study, we report its association with the TGFb1 signaling pathway, which promotes epithelial-mesenchymal transition (EMT) in breast cancer. SND1 was upregulated in breast cancer tissues, in particular in primary invasive ductal carcinomas. Transcriptional activation of the SND1 gene was controlled by the TGFb1/Smad pathway, specifically by activation of the Smad2/Smad3 complex. The SND1 promoter region contained several Smad-specific recognition domains (RD motifs), which were recognized and bound by the Smad complex that enhanced the transcriptional activation of SND1. We found that SND1 promoted expression of the E3 ubiquitin ligase Smurf1, leading to RhoA ubiquitination and degradation. RhoA degradation in breast cancer cells disrupted F-actin cytoskeletal organization, reduced cell adhesion, increased cell migration and invasion, and promoted metastasis. Overall, our results define a novel role for SND1 in regulating breast tumorigenesis and metastasis. Cancer Res; 75(7); 1275-86. Ó2015 AACR.

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Section: Introductionmentioning

confidence: 99%

SND1 Acts Downstream of TGFβ1 and Upstream of Smurf1 to Promote Breast Cancer Metastasis

Liu

Cui

et al. 2015

Cancer Research

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“…In addition, in a breast cancer model, SND1 is required for the expansion and activity of tumor-initiating cells (16). We also reported earlier that SND1 can form a loop with SMAD family members and reciprocally regulate the promotion of breast cancer metastasis through a TGF-b-signaling pathway (17)(18)(19). As a multifunctional protein, it is likely that SND1 regulates diverse signal pathways involved in proliferation and metastasis in different cancers (20,21).…”

mentioning

confidence: 59%

“…In support of our data, Arretxe et al (25) showed that SND1 was potentially able to recognize the promoter region of SLUG through ChIP-on-chip assays. In our previous study, we likewise found that SLUG is a target promoter of SND1 by ChIP-guided ligation and selection assay (17). We therefore performed experiments to discover the potential role of SND1 in regulating the gene transcriptional activation of SLUG, which further affects the expression of epithelial markers.…”

Section: Snd1 Activates Slug Transcription By Increasing Chromatin Acmentioning

confidence: 86%

SND1 acts upstream of SLUG to regulate the epithelial–mesenchymal transition (EMT) in SKOV3 cells

et al. 2018

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Staphylococcal nuclease domain‐containing protein 1 (SND1) has been reported as an oncoprotein in a variety of cancers involving multiple processes, including proliferation, angiogenesis, and metastasis. However, the mechanisms underlying metastasis remain largely unknown. Herein, by using the ovarian cancer cell line SKOV3, which has high metastasis ability, we showed that loss‐of‐function of SND1 dramatically suppressed the invasion and migration of SKOV3 cells. We then performed gene expression profiles and further verified (by use of quantitative PCR and Western blot analysis) that loss‐of‐function of SND1 resulted in up‐regulation of epithelial markers, such as epithelial cadherin and claudin 1, and down‐regulation of mesenchymal markers, including neural cadherin and vimentin. Moreover, we illustrated that SLUG, a key transcription factor implicated in epithelial–mesenchymal transition and metastasis, acts as an essential effector of the SND1‐promoted epithelial–mesenchymal transition process via regulating N‐CAD and VIM expression (or E‐CAD and CLDN1). The underlying molecular mechanisms illustrated that SND1 regulates the gene transcriptional activation of SLUG by increasing chromatin accessibility through the recruitment of the acetyltransferases GCN5 and CBP/p300 to the SLUG promoter proximal region. Overall, SND1 was identified as a novel upstream regulator of SLUG, which plays important roles in regulating the E‐CAD/N‐CAD expression switch.—Xin, L., Zhao, R., Lei, J., Song, J., Yu, L., Gao, R., Ha, C., Ren, Y., Liu, X., Liu, Y., Yao, Z., Yang, J. SND1 acts upstream of SLUG to regulate the epithelial‐mesenchymal transition (EMT) in SKOV3 cells. FASEB J. 33, 3795–3806 (2019). http://www.fasebj.org

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“…23 This domain has been reported to recognize and bind methylated lysine and arginine of target proteins, which is a key factor for their ability to facilitate the assembly of larger protein complexes at discrete cellular compartments. [24][25][26][27][28][29] It seems that a common function of proteins containing Tudor domain, including TSN, is to act as an adaptor in order to link methylated arginine or lysine to effector molecules with specific catalytic activities. 24 It has recently been shown that human TSN interacts through its Tudor domain with core components of RNA splicing machinery, including Prp8 (human U5-220 kD Protein), two Sm proteins, SmB and SmD1/D3 and the splicing factor SAM68 (Src-associated in mitosis of 68 kDa).…”

Section: Structure and Intracellular Localization Of Tsn: Clues To Mumentioning

confidence: 99%

“…6,7 Accordingly, a set of TSN-bound promoter regions has been recently identified using chromatin immunoprecipitation. 26 The interaction of TSN with multiple components of transcription machinery makes it an important factor in the regulation of a plethora of cellular signaling pathways implicated in the pathogenesis of various human diseases.…”

Section: Structure and Intracellular Localization Of Tsn: Clues To Mumentioning

confidence: 99%

Tudor staphylococcal nuclease: biochemistry and functions

et al. 2016

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Tudor staphylococcal nuclease (TSN, also known as Tudor-SN, SND1 or p100) is an evolutionarily conserved protein with invariant domain composition, represented by tandem repeat of staphylococcal nuclease domains and a tudor domain. Conservation along significant evolutionary distance, from protozoa to plants and animals, suggests important physiological functions for TSN. It is known that TSN is critically involved in virtually all pathways of gene expression, ranging from transcription to RNA silencing. Owing to its high protein-protein binding affinity coexistent with enzymatic activity, TSN can exert its biochemical function by acting as both a scaffolding molecule of large multiprotein complexes and/or as a nuclease. TSN is indispensible for normal development and stress resistance, whereas its increased expression is closely associated with various types of cancer. Thus, TSN is an attractive target for anti-cancer therapy and a potent tumor marker. Considering ever increasing interest to further understand a multitude of TSN-mediated processes and a mechanistic role of TSN in these processes, here we took an attempt to summarize and update the available information about this intriguing multifunctional protein. TSN is an evolutionarily conserved protein having a pivotal role in the regulation of gene expression. TSN acts both as a scaffolding protein and as a nuclease. TSN sustains cell viability and its cleavage by proteases facilitates cell death. TSN is implicated in key cancer-related processes and is a potent marker of various types of tumors. Open questions:How is nucleolytic activity of TSN regulated in vivo and how this affects interaction of TSN with downstream targets? What are the structural bases and functional consequences of distinct intracellular localization patterns of TSN in animals and plants? What are the molecular mechanisms of the TSN-mediated cancerogenesis?God has given you one face, and you make yourself another (William Shakespeare). Being true for all living organisms, accurate spatio-temporal regulation of gene expression is a fundamental mechanism underlying development, homeostasis and adaptation to the environment. Eukaryotic gene expression is a cumulative outcome of a multitude of molecular processes, including transcription, mRNA splicing, stability and translation, chromatin modification, as well as protein stability and modification. Each of these processes is in turn controlled by a highly dedicated repertoire of proteins. However, one protein, Tudor staphylococcal nuclease (TSN, also known as Tudor-SN, SND1 or p100) appears to act in most of the gene expression pathways.TSN is an evolutionarily conserved protein found in all eukaryotic lineages, except budding yeast, Saccharomyces cerevisiae. Conservation along significant evolutionary distance suggests important physiological functions for TSN. Invariant domain composition of TSN comprises tandem repeat of four staphylococcal nuclease (SN)-like domains (hereafter referred to as SN domains) at the N terminus and a fusio...

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Identification of p100 target promoters by chromatin immunoprecipitation-guided ligation and selection (ChIP-GLAS)

Cited by 13 publications

References 12 publications

SND1 Acts Downstream of TGFβ1 and Upstream of Smurf1 to Promote Breast Cancer Metastasis

SND1 Acts Downstream of TGFβ1 and Upstream of Smurf1 to Promote Breast Cancer Metastasis

SND1 acts upstream of SLUG to regulate the epithelial–mesenchymal transition (EMT) in SKOV3 cells

Tudor staphylococcal nuclease: biochemistry and functions

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