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Suppression of programmed death and G 1 arrest in B‐cell hybridomas by interleukin‐6 is not accompanied by altered expression of immediate early response genes
Author(s) -
Sabourin Luc A.,
Hawley Robert G.
Publication year - 1990
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041450325
Subject(s) - biology , programmed cell death , microbiology and biotechnology , signal transduction , northern blot , cell cycle , cell growth , viability assay , gene expression , gene , cell , apoptosis , biochemistry
The murine B‐cell hybridoma B9 requires interleukin‐6 (IL‐6) for its survival and proliferation in vitro. We show here that withdrawal of IL‐6 from B9 cultures results in programmed death, concomitant with arrest of the cells in the G 1 phase of the cell cycle. Unlike several other systems that undergo programmed cell death, no induction of transcripts corresponding to the testosterone‐repressed message‐2 or transglutaminase genes is observed during this process. Upon readdition of IL‐6 to G 1 ‐arrested B9 cells, viability is maintained and entry into S phase occurs after a lag period of 10 to 12 hr. Northern blot analysis showed that the immediate‐early mRNAs normally induced shortly after growth factor stimulation in quiescent fibroblasts (c‐fos, c‐jun, Egr‐1, c‐myc, JE , and KC), and other growth‐related genes (2F1, c‐Ha‐ras, and p53), are either not induced or remain unchanged during G 1 to S phase progression. A correlation was found, however, between the temporal pattern of expression of several G 1 /S phase genes (dihy‐drofolate reductase, thymidine kinase, transferrin receptor, and histone H3) and DNA synthesis. These results demonstrate that IL‐6‐induced viability and growth of hybridoma (and, presumably, plasmacytoma) cells is mediated via novel signal transduction pathways.