Highly-expressed p100/p52 (NFKB2) sequesters other NF-κB-related proteins in the cytoplasm of human breast cancer cells

E. Dejardin, G. Bonizzi, A. Bellahcene, V. Castronovo, M. P. Merville, V. Bours

Research output: Contribution to journalArticle

Abstract

Several observations have suggested that NF-κB transcription factors could be involved in carcinogenesis. To investigate the possibility that members of the NF-κB family participate in the molecular control of the transformed phenotype, we examined the expression of these proteins in human breast cancer cell lines as well as in primary tumors. Western Immunoblots demonstrated high expression of the p52 precursor p100 (NFKB2) in several breast cancer cell lines while human mammary epithelial cells express this protein only faintly. Eighteen primary breast tumors out of 24 displayed significant expression of the p100/p52 protein. In MDA-MB-435 cells, overexpressed p100 and p52 are predominantly cytoplasmic and coimmunoprecipitation experiments demonstrated that p100 sequesters the heterodimer p50/ p65 in the cytoplasm. We demonstrate that most p65 protein is complexed with p100 in these cells while it is complexed predominantly with Iκ-B-α in cell lines expressing less p100. Our data strengthen the hypothesis that NF-κB could be involved in carcinogenesis and suggest that the p100/p52 NF-κB subunit could play a role in the development of human breast cancers, possibly by sequestering other NF-κB-related proteins in the cytoplasm.

Original languageEnglish
Pages (from-to)1835-1841
Number of pages7
JournalOncogene
Volume11
Issue number9
Publication statusPublished - 1995

Keywords

  • Breast cancer
  • NF-κB
  • NFKB2
  • Transcription factors

ASJC Scopus subject areas

  • Cancer Research
  • Genetics
  • Molecular Biology

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  • Cite this

    Dejardin, E., Bonizzi, G., Bellahcene, A., Castronovo, V., Merville, M. P., & Bours, V. (1995). Highly-expressed p100/p52 (NFKB2) sequesters other NF-κB-related proteins in the cytoplasm of human breast cancer cells. Oncogene, 11(9), 1835-1841.