Cdx2 and the Brm-type SWI/SNF complex cooperatively regulate villin expression in gastrointestinal cells

Yamamichi, Nobutake; Inada, Ken Ichi; Furukawa, Chihiro; Sakurai, Kouhei; Tando, Toshio; Ishizaka, Aya; Haraguchi, Takeshi; Mizutani, Taketoshi; Fujishiro, Mitsuhiro; Shimomura, Ryoichi; Oka, Masashi; Ichinose, Masakazu; Tsutsumi, Yutaka; Omata, Masao; Iba, Hideo

doi:10.1016/j.yexcr.2009.01.006

Cited by 34 publications

(60 citation statements)

References 41 publications

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“…A recent study found that knockdown of CDX2 in SW480 cells caused a clear down regulation of villin. Indicated that villin is regulated by CDX2 (Yamamichi et al, 2009). Therefore, some investigators suggest to use both CDX2 and Villin as markers for the detection of early IM and supplements for the histologic diagnosis of BE.…”

Section: Discussionmentioning

confidence: 99%

“…Immunohistochemical analyses of gastric intestinal metaplasia and cancer revealed that villin and Cdx2 expression are tightly coupled. Both of them are demonstrated to be useful maker for the diagnosis of Barrett's esophagus and intestinal metastasis in stomach (Dudouet et al, 1987;Fitzgerald et al, 1997;Athman et al, 2002;Niwa et al, 2005;Shi et al, 2008;Yamamichi et al, 2009).…”

Section: Expression Of Cdx2 and Villin In Gastric Cardiac Intestinal mentioning

confidence: 99%

See 1 more Smart Citation

Expression of CDX2 and Villin in Gastric Cardiac Intestinal Metaplasia and the Relation with Gastric Cardiac Carcinogenesis

Xiao¹,

Ru²,

Sun³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Section: Discussionmentioning

confidence: 99%

Section: Expression Of Cdx2 and Villin In Gastric Cardiac Intestinal mentioning

confidence: 99%

Expression of CDX2 and Villin in Gastric Cardiac Intestinal Metaplasia and the Relation with Gastric Cardiac Carcinogenesis

Xiao¹,

Ru²,

Sun³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…Importantly, transactivation mediated through RelA/p50 (Fig. 1C, lanes 14 -18 compared with lane 13), RelB/p52 (lanes 20 -24 compared with lane 19), and c-Rel/p50 (lanes 8 -12 compared with lane 7) was enhanced by the endogenous expression of any of the five candidate proteins (lanes [7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24]. No significant differences were found among these five proteins in terms of the enhancement of any of the three NF-B dimers, suggesting that all potentially function as co-activators of NF-B in any context, at least when expressed at high levels.…”

Section: High Expression Of Each Member Of the D4 Family And Phf10mentioning

confidence: 99%

“…The SWI/SNF complex has two alternative ATPases, Brahma (Brm) or Brahma-related gene 1 (BRG1) as the catalytic subunits, and other subunits such as BAF155, Ini1/SNF5, BAF170, BAF60a, and ␤-actin (8 -10). The SWI/SNF complex is recruited to target genes via association with transcription regulators such as c-Myc (11), C/EBP␤ (12), AP-1 (13), neuron-restrictive silencer factor (14), and Cdx2 (15). In addition to cellular targets, we have shown that integrated LTRs of murine leukemia virus (16,17) and HIV-1 (human immunodeficiency virus-1) (18) require the Brm-type SWI/SNF complex to maintain their gene expression.…”

Section: Nf-bmentioning

confidence: 99%

Double Plant Homeodomain (PHD) Finger Proteins DPF3a and -3b Are Required as Transcriptional Co-activators in SWI/SNF Complex-dependent Activation of NF-κB RelA/p50 Heterodimer

Ishizaka

Mizutani

Kobayashi

et al. 2012

Journal of Biological Chemistry

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Background:The NF-B dimer, RelA/p50, often requires the SWI/SNF complex for its transactivation function, but its molecular mechanisms remain elusive. Results: The NF-B canonical pathway induced by TNF-␣ is DPF3a/b-and SWI/SNF-dependent for some promoters. Conclusion: DPF3a and DPF3b are effective linkers for the SWI/SNF complex and RelA/p50. Significance: The NF-B⅐DPF3a/b⅐SWI/SNF complex would be an effective platform for promoter-specific transactivation.

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“…For example, Brm-type, but not BRG1-type, SWI/SNF complexes are essential for the maintenance of gene expression driven by the long terminal repeats of murine leukemia virus (5,6) and human immunodeficiency virus (7). Moreover, in gastrointestinal cells, Brm but not BRG1 can transactivate Cdx2-dependent villin expression, even though both proteins can interact with Cdx2 (8). Overall, the SWI/SNF complexes interact with various proteins, including transcriptional regulators, through the many specific and varied associations with their subunits.…”

mentioning

confidence: 99%

Requiem Protein Links RelB/p52 and the Brm-type SWI/SNF Complex in a Noncanonical NF-κB Pathway

Tando

Ishizaka

Watanabe

et al. 2010

Journal of Biological Chemistry

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The SWI/SNF chromatin remodeling complex plays pivotal roles in mammalian transcriptional regulation. In this study, we identify the human requiem protein (REQ/DPF2) as an adaptor molecule that links the NF-B and SWI/SNF chromatin remodeling factor. Through in vitro binding experiments, REQ was found to bind to several SWI/SNF complex subunits and also to the p52 NF-B subunit through its nuclear localization signal containing the N-terminal region. REQ, together with Brm, a catalytic subunit of the SWI/SNF complex, enhances the NF-Bdependent transcriptional activation that principally involves the RelB/p52 dimer. Both REQ and Brm were further found to be required for the induction of the endogenous BLC (CXCL13) gene in response to lymphotoxin stimulation, an inducer of the noncanonical NF-B pathway. Upon lymphotoxin treatment, REQ and Brm form a larger complex with RelB/p52 and are recruited to the BLC promoter in a ligand-dependent manner. Moreover, a REQ knockdown efficiently suppresses anchorageindependent growth in several cell lines in which the noncanonical NF-B pathway was constitutively activated. From these results, we conclude that REQ functions as an efficient adaptor protein between the SWI/SNF complex and RelB/p52 and plays important roles in noncanonical NF-B transcriptional activation and its associated oncogenic activity.The SWI/SNF (switch/sucrose-nonfermentable) chromatin remodeling complex has important functional roles in the epigenetic regulation of many organisms and regulates a wide variety of genes (1, 2). In mammals, this complex is an assembly of about nine polypeptides and contains a single molecule of either Brm or BRG1 but not both (3). These two proteins are the catalytic subunits that together with noncatalytic subunits, such as BAF170, BAF155, Ini1, BAF60a, and ␤-actin, drive the remodeling of nucleosomes via their ATP-dependent helicase activity (4). Evidence has now accumulated that the Brm-type and BRG1-type SWI/SNF complexes regulate a set of target promoters that do not fully overlap. Indeed, Brm and BRG1 show clear differences in their biological activities. For example, Brm-type, but not BRG1-type, SWI/SNF complexes are essential for the maintenance of gene expression driven by the long terminal repeats of murine leukemia virus (5, 6) and human immunodeficiency virus (7). Moreover, in gastrointestinal cells, Brm but not BRG1 can transactivate Cdx2-dependent villin expression, even though both proteins can interact with Cdx2 (8). Overall, the SWI/SNF complexes interact with various proteins, including transcriptional regulators, through the many specific and varied associations with their subunits. We previously demonstrated that among all of the dimers formed between Fos and Jun family proteins, which compose the representative transcription factor AP-1, the c-Fos/c-Jun heterodimer most efficiently recruits SWI/SNF complexes to AP-1-binding sites through its specific binding activity to the BAF60a SWI/SNF subunit (9).Like AP-1, the NF-B 3 is an important transcription facto...

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Cdx2 and the Brm-type SWI/SNF complex cooperatively regulate villin expression in gastrointestinal cells

Cited by 34 publications

References 41 publications

Expression of CDX2 and Villin in Gastric Cardiac Intestinal Metaplasia and the Relation with Gastric Cardiac Carcinogenesis

Expression of CDX2 and Villin in Gastric Cardiac Intestinal Metaplasia and the Relation with Gastric Cardiac Carcinogenesis

Double Plant Homeodomain (PHD) Finger Proteins DPF3a and -3b Are Required as Transcriptional Co-activators in SWI/SNF Complex-dependent Activation of NF-κB RelA/p50 Heterodimer

Requiem Protein Links RelB/p52 and the Brm-type SWI/SNF Complex in a Noncanonical NF-κB Pathway

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