Steroid- and retinoid-mediated growth arrest and apoptosis in WEHI-231 cells: Role of NF-κB, c-Myc and CKI p27(Kip1)

Dubravka Donjerković, Carolyn M. Mueller, David W. Scott*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


IgM cross-linking induces NF-κB inactivation, c-Myc down-regulation, and cyclin kinase inhibitor p27(Kip1) accumulation in WEHI-231 murine B lymphoma cells. p27(Kip1) up-regulation leads to a decreased cyclin-dependent kinase 2 activity, retinoblastoma protein hypophosphorylation, G1 arrest and apoptosis. Similar to membrane (m) IgM cross-linking in B lymphoma cells, steroids and retinoids down-regulate c-Myc (via NF-κB inactivation) and induce apoptosis in T cell hybridomas and thymocytes. In this study, we determined if steroids and retinoids have similar effects in WEHI-231 cells. Our results show that steroids and retinoids induce NF-κB inactivation, c-Myc down-regulation, p27(Kip1) up-regulation, G1 arrest, and apoptosis. Importantly, these hormones enhance anti-IgM-induced apoptosis in WEHI-231 cells. Similar to mIgM signaling, all these effects are prevented by treatment with CD40 ligand. Caspase inhibition, on the other hand, rescues cells from steroid/retinoid-induced apoptosis, but has no effect on growth arrest, p27(Kip1), and c-Myc. Together, these findings suggest that steroids/retinoids and mIgM cross-linking share a common signal transduction pathway leading to G1 arrest and cell death.

Original languageEnglish
Pages (from-to)1154-1161
Number of pages8
JournalEuropean Journal of Immunology
Issue number4
StatePublished - 2000
Externally publishedYes


  • Apoptosis
  • B lymphocyte
  • Cellular proliferation


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