Jurkat cells respond to biotin deficiency with increased nuclear translocation of NF-κB, mediating cell survival

Rocio Rodriguez-Melendez, Lyndsay D. Schwab, Janos Zempleni

Research output: Contribution to journalArticlepeer-review

28 Scopus citations

Abstract

Members of the NF-κB family of transcription factors cause transcriptional, activation of anti-apoptotic genes. Here we determined whether survival of biotin-deficient cells is mediated by nuclear translocation of NF-κB. Human T (Jurkat) cells were cultured in biotin-deficient or biotin-supplemented media; nuclear translocation of NF-κB was stimulated with phytohemagglutinin and phorbol-12-myristate-13-acetate. Nuclear abundance of two members (p50 and p65) of the NF-κB family was greater in biotin-deficient compared to biotinsupplemented cells; this effect was mediated by phosphorylation of IκBα. The nuclear enrichment of p50 and p65 in biotin-deficient cells was associated with transcriptional activation of NF-κB-dependent genes such as the tumor suppressor gene p53 and the anti-apoptotic gene Bfl-1/A1. Biotin-deficient cells exhibited smaller activities of the apoptotic enzyme caspase-3 in response to treatment with tumor necrosis factor α, and decreased cell death in response to serum starvation compared to biotin-supplemented cells. These findings suggest that NF-κB mediates survival of biotin-deficient cells.

Original languageEnglish (US)
Pages (from-to)209-216
Number of pages8
JournalInternational Journal for Vitamin and Nutrition Research
Volume74
Issue number3
DOIs
StatePublished - May 2004

Keywords

  • Apoptosis
  • Bfl-1/A1
  • Cells
  • Human
  • Jurkat
  • P53

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Endocrinology, Diabetes and Metabolism
  • Nutrition and Dietetics

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