Differential roles for the coactivators CBP and p300 on TCF/β-catenin-mediated survivin gene expression

Ma, Hong; Nguyen, Carvell T.; Lee, Kyung-Soon; Kahn, Michaël

doi:10.1038/sj.onc.1208433

Cited by 291 publications

(316 citation statements)

References 45 publications

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“…HGFR activation protects from apoptosis in several tumor in vitro models (Bowers et al, 2000;Fan et al, 2000Fan et al, , 2005Gao et al, 2001;Zeng et al, 2002;Derksen et al, 2003;Lal et al, 2005), and activation of b-catenin promotes the transcription of antiapoptotic genes (Dihlmann et al, 2005;Kim et al, 2005;Ma et al, 2005) and was associated with increased tumor cell survival in CRC (Ireland et al, 2004;Ougolkov et al, 2004). However, a proapoptotic role of HGF (Arakaki et al, 1998;Matteucci et al, 2003;Rasola et al, 2004) and b-catenin (Kim et al, 2000;van Gijn et al, 2001;Edlund et al, 2005) was also reported in several models.…”

Section: Discussionmentioning

confidence: 99%

A positive feedback loop between hepatocyte growth factor receptor and β-catenin sustains colorectal cancer cell invasive growth

et al. 2006

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Overexpressed or activated hepatocyte growth factor receptor, encoded by the MET proto-oncogene, was found in the majority of colorectal carcinomas (CRCs), whose stepwise progression to malignancy requires transcriptional activation of b-catenin. We here demonstrate that a functional crosstalk between Met and b-catenin signaling sustains and increases CRC cell invasive properties. Hepatocyte growth factor (HGF) stimulation prompts b-catenin tyrosine phosphorylation and dissociation from Met, and upregulates b-catenin expression via the phosphatidylinositol 3-kinase pathway in conditions that mimic those found by the invading and metastasizing cells. Additionally, a transcriptionally active form of b-catenin, known to be oncogenic, enhances Met expression. Furthermore, HGF treatment increases the activity of the b-catenin-regulated T-cell factor transcription factor in cells expressing the wild-type or the oncogenic b-catenin. In the mirror experiments, either Met or b-catenin knocking down also reduces their protein level. In biological assays, b-catenin knocking down abrogates the HGF-induced motile phenotype, whereas active b-catenin fosters ligand-independent cell scattering. Met and b-catenin also cooperate in promoting entry into the cell cycle and in protecting cells from apoptosis. In conclusion, Met and b-catenin pathways are mutually activated in CRC cells. This might generate a selfamplifying positive feedback loop resulting in the upregulation of the invasive growth properties of CRC cells.

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Section: Discussionmentioning

confidence: 99%

A positive feedback loop between hepatocyte growth factor receptor and β-catenin sustains colorectal cancer cell invasive growth

et al. 2006

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“…Sumoylation of the CRD1 domain of p300 was shown to mediate this repressor activity. In vitro and in vivo studies suggested that a direct binding of HDAC6 to SUMO-CRD1 could be responsible for the observed transcription repression by the CRD1 domain of p300 (Girdwood et al, 2003), and further investigations suggested that this mechanism could be involved in the repression of at least two cellular genes (Ling and Lobie, 2004;Ma et al, 2005).…”

Section: Nuclear Targets Of Hdac6mentioning

confidence: 98%

HDAC6, at the crossroads between cytoskeleton and cell signaling by acetylation and ubiquitination

et al. 2007

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Histone deacetylase 6 (HDAC6) is a unique enzyme with specific structural and functional features. It is actively or stably maintained in the cytoplasm and is the only member, within the histone deacetylase family, that harbors a full duplication of its deacetylase homology region followed by a specific ubiquitin-binding domain at the C-terminus end. Accordingly, this deacetylase functions at the heart of a cellular regulatory mechanism capable of coordinating various cellular functions largely relying on the microtubule network. Moreover, HDAC6 action as a regulator of the HSP90 chaperone activity adds to the multifunctionality of the protein, and allows us to propose a critical role for HDAC6 in mediating and coordinating various cellular events in response to different stressful stimuli.

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“…27 It has been shown that it plays a very distinct role in survivin gene transcription. 28 The direct inhibition of survivin expression by curcumin was shown very recently in adult T-cell leukemia. 8 Also our data (Wolanin et al, accepted to Mol.…”

Section: Discussionmentioning

confidence: 99%

Resistance to apoptosis of HCW‐2 cells can be overcome by curcumin‐ or vincristine‐induced mitotic catastrophe

Magalska

Śliwińska

Szczepanowska

et al. 2006

Intl Journal of Cancer

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The term mitotic catastrophe has recently become widely used to describe a form of death affecting many cancer cells, which, because of severe DNA or mitotic spindle damage, are not able to bypass mitosis. We show here that cells of the HL-60-derived HCW-2 line highly resistant to apoptosis, upon treatment with curcumin or vincristine, undergo mitotic catastrophe that is finalized by caspase 3 activation and oligonucleosomal DNA degradation. Curcumin is a natural dye, derived from Curcuma longa that has been shown to induce cell death in many cancer cells. Both treatments decrease cell proliferation and cell survival, arrest cells in G 2 /M phase of cell cycle and induce morphological changes characterized by cell enlargement and micronucleation. ''Catastrophic'' cells comprise a separate subpopulation with less than 4 C DNA, as evidenced by flow and scanning cytometry. This subpopulation is MPM-2 positive. Thymidine block increased the number of cell arrested in the G 2 /M phase of cell cycle and curcumin effectiveness as an inducer of mitotic catastrophe. Curcumin, but not vincristine, acts on HCW-2 cells by inhibiting the expression of survivin, a modulator of cell division and apoptosis in cancer. Altogether our results show that apoptosis resistance can be overcome by inducing mitotic catastrophe in HCW-2 cells. ' 2006 Wiley-Liss, Inc.

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Differential roles for the coactivators CBP and p300 on TCF/β-catenin-mediated survivin gene expression

Cited by 291 publications

References 45 publications

A positive feedback loop between hepatocyte growth factor receptor and β-catenin sustains colorectal cancer cell invasive growth

A positive feedback loop between hepatocyte growth factor receptor and β-catenin sustains colorectal cancer cell invasive growth

HDAC6, at the crossroads between cytoskeleton and cell signaling by acetylation and ubiquitination

Resistance to apoptosis of HCW‐2 cells can be overcome by curcumin‐ or vincristine‐induced mitotic catastrophe

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