Curcumin causes the growth arrest and apoptosis of B cell lymphoma by downregulation of egr-1, C-myc, Bcl-X(l), NF-κB, and p53

Seong Su Han, Seung Tae Chung, Darrell A. Robertson, Dinesh Ranjan, Subbarao Bondada

Research output: Contribution to journalArticlepeer-review

201 Scopus citations

Abstract

It has been well known that curcumin is a powerful inhibitor of proliferation of several tumor cells. However, the molecular basis of the anti-proliferative effect of curcumin has not been investigated in detail. In this paper, we present evidence to show that curcumin inhibited proliferation of a variety of B lymphoma cells. At low concentrations curcumin inhibited the proliferation of BKS-2, an immature B cell lymphoma, more effectively than that of normal B lymphocytes and caused the apoptosis of BKS-2 cells in a dose- and time-dependent manner. Furthermore, curcumin downregulated the expression of survival genes egr-1, c-myc, and bcl-X(L) as well as the tumor suppressor gene p53 in B cells. In addition, NF-κB binding activity was also downregulated almost completely by curcumin. Stimulation with CpG oligonucleotides or anti-CD40 overcame growth inhibition induced by low concentrations of curcumin. Our results suggest that curcumin caused the growth arrest and apoptosis of BKS-2 immature B cell lymphoma by downregulation of growth and survival promoting genes.

Original languageEnglish (US)
Pages (from-to)152-161
Number of pages10
JournalClinical Immunology
Volume93
Issue number2
DOIs
StatePublished - Nov 1999

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

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