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A role for CITED2, a CBP/p300 interacting protein, in colon cancer cell invasion.

Longchuan Bai | Juanita L Merchant
FEBS letters | 2007

A thorough understanding of histone acetyltransferase CBP/p300-mediated regulation of gene expression and cell growth is essential to identify mechanisms relevant to the development of histone deacetylase (HDAC) inhibitor-based preventive and therapeutic strategies. We found that knockdown of CBP/p300 interacting coactivator with glutamic acid/aspartic acid-rich tail 2 (CITED2) increased colon cancer cell invasiveness in vitro. Gene expression profiling revealed that CITED2 knockdown induced matrix metalloproteinase-13 (MMP-13) gene expression in colon cancer cells. Butyrate, a naturally occurring HDAC inhibitor, induced CITED2 expression and downregulated MMP-13 expression in RKO cells. Additionally, ectopic expression of CITED2 arrested RKO cell growth. Thus, CITED2 regulates colon cancer invasion and might be a target for HDAC inhibitor-based intervention of colon cancer.

Pubmed ID: 18054336

Research resources used in this publication

None found

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Associated grants

  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK055732-08
  • Agency: NCI NIH HHS, United States
    Id: P30 CA046592
  • Agency: NIDDK NIH HHS, United States
    Id: P30 DK034933
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK055732
  • Agency: NIDDK NIH HHS, United States
    Id: P30-DK34933
  • Agency: NIDDK NIH HHS, United States
    Id: R01-DK55732

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AnaSpec (tool)

RRID:SCR_002114

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SPOT - Biological prioritization after a SNP association study (tool)

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