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β-catenin interacts with and inhibits NF-κB in human colon and breast cancer

  • Jiong Deng
  • , Stephanie A. Miller
  • , Hong Ying Wang
  • , Weiya Xia
  • , Yong Wen
  • , Binhua P. Zhou
  • , Yan Li
  • , Shiaw Yih Lin
  • , Mien Chie Hung

Producción científica: Articlerevisión exhaustiva

350 Citas (Scopus)

Resumen

β-catenin plays an important role in development and homeostasis. Deregulated β-catenin is involved in oncogenesis. In this study, we found that β-catenin can physically complex with NF-κB, resulting in a reduction of NF-κB DNA binding, transactivation activity, and target gene expression. Repressed NF-κB activity is found in human colon cancer cells in which β-catenin is activated. Importantly, activated β-catenin was found to inhibit the expression of NF-κB target genes, including Fas and TRAF1. Furthermore, a strong inverse correlation was identified between the expression levels of β-catenin and Fas in colon and breast tumor tissues, suggesting that β-catenin regulates NF-κB and its targets in vivo. Thus, β-catenin may play an important role in oncogenesis through the crossregulation of NF-κB.

Idioma originalEnglish
Páginas (desde-hasta)323-334
Número de páginas12
PublicaciónCancer Cell
Volumen2
N.º4
DOI
EstadoPublished - oct 2002

Nota bibliográfica

Funding Information:
This work was supported by NIH grants CA58880 and Ovarian SPORE grant P50 CA83639 (to M.-C. Hung), by a predoctoral fellowship from the US Army Breast Cancer Research Training Grant Program, Grant No. DAMD17-99-1-9264 (to Y. Wen), and Grant No. DAMD 17-02-1-0454 (to Y. Li). We would like to thank Dr. S.W. Byers for the wild type β-catenin and β-cateninS37A plasmids, Dr. H. Clevers for the dominant negative TCF4 (pcDNA3-ΔNTCF4), TOP, and FOP plasmids, and Dr. L.K. Su for the APC expression plasmid. We would also like to thank Dr. A.G. de Herreros for the GST-β-catenin, Dr. P.J. Chiao for the pBS-p65 and pBS-p105 and MEF rela −/− cells, and Dr. J. Schmid for the GFP-p65 plasmid.

Financiación

This work was supported by NIH grants CA58880 and Ovarian SPORE grant P50 CA83639 (to M.-C. Hung), by a predoctoral fellowship from the US Army Breast Cancer Research Training Grant Program, Grant No. DAMD17-99-1-9264 (to Y. Wen), and Grant No. DAMD 17-02-1-0454 (to Y. Li). We would like to thank Dr. S.W. Byers for the wild type β-catenin and β-cateninS37A plasmids, Dr. H. Clevers for the dominant negative TCF4 (pcDNA3-ΔNTCF4), TOP, and FOP plasmids, and Dr. L.K. Su for the APC expression plasmid. We would also like to thank Dr. A.G. de Herreros for the GST-β-catenin, Dr. P.J. Chiao for the pBS-p65 and pBS-p105 and MEF rela −/− cells, and Dr. J. Schmid for the GFP-p65 plasmid.

FinanciadoresNúmero del financiador
National Institutes of Health (NIH)DAMD17-99-1-9264, DAMD 17-02-1-0454, CA58880
National Institutes of Health (NIH)
National Childhood Cancer Registry – National Cancer InstituteP50CA083639
National Childhood Cancer Registry – National Cancer Institute

    ODS de las Naciones Unidas

    Este resultado contribuye a los siguientes Objetivos de Desarrollo Sostenible

    1. Good health and well being
      Good health and well being

    ASJC Scopus subject areas

    • Oncology
    • Cancer Research

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