Distinct IL-6 signal transduction leads to growth arrest and death in B cells or growth promotion and cell survival in myeloma cells

W. C. Cheung, B. Van Ness

Research output: Contribution to journalArticlepeer-review

49 Scopus citations

Abstract

In B cell development, interleukin-6 (IL-6) induces terminal maturation of B lymphocytes into antibody producing plasma cells. Terminal differentiated B cells cell cycle arrest and death follows. In contrast, IL-6 acts as a growth factor for malignant myeloma plasma cells and in some cases protects them from therapeutic treatment. In this study, we examined two cell lines that show different responses to IL-6. Lymphoblastoid CESS cells respond to IL-6 by terminally differentiating into antibody producing plasma cells, cell cycle arrest, and undergo cell death. Continuous addition of IL-6 to these cells induces transient activation of STAT3, SHP-2 phosphorylation, and does not alter bcl-XL and c-myc expression. In contrast, the myeloma line ANBL6 proliferates when stimulated with IL-6 and this correlates with prolonged STAT3 activation and up-regulation of bcl-XL and c-myc. Interestingly, gp130-associated SHP-2 phosphorylation was detected in the IL-6-induced CESS cells but not myeloma cell lines. The data show a very distinct IL-6 signal transduction and kinetics in these cell lines and the distinct molecular events correlate closely to the cell fate of the lymphoblast and myeloma cell lines.

Original languageEnglish (US)
Pages (from-to)1182-1188
Number of pages7
JournalLeukemia
Volume16
Issue number6
DOIs
StatePublished - 2002

Bibliographical note

Funding Information:
This work was supported by NIH grants CA21115 to the Eastern Cooperative Oncology Group and CA62242.

Keywords

  • IL-6 signal transduction
  • Multiple myeloma
  • STAT3

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