V-ABL does not abolish IL-6 requirement by murine plasmacytoma cells
✍ Scribed by Hiroyuki Sugiyama; Francis Wiener; Magda Babonits; Santiago Silva; Toshio Hirano; Tadamitsu Kishimoto; George Klein
- Book ID
- 102868760
- Publisher
- John Wiley and Sons
- Year
- 1991
- Tongue
- French
- Weight
- 512 KB
- Volume
- 48
- Category
- Article
- ISSN
- 0020-7136
No coin nor oath required. For personal study only.
✦ Synopsis
Activation of c-myc by juxtaposition to an immunoglobulin locus and introduction of the v-abl oncogene act synergistically in generating a mouse plasmacytoma (PC). The question arose whether the effect of v-abl could be attributed to a deregulation of interleukin-6 (11-6) production or responsiveness, in view of the fact that IL-6 exerts potent growthstimulatory activity on PC cells. We studied the effect of IL-6 on the in vitro growth of primary PCs induced by pristane
alone (TEPCs) or by pristane + A-MuLV (ABPCs). Five of I3
TEPCs and 3 of 7 ABPCs responded to IL-6. Macrophage supernatants prepared from both TEPCs and ABPCs had similar stimulatory effects on PC cells. From 30 primary PCs (including both TEPCs and ABPCs), we established 9 in vitro lines, 2 of which expressed v-abl. All were able to grow on macrophage feeder layers. Three types of behavior could be distinguished on the basis of growth in feeder-free cultures in the presence and absence of 11-6. Group I contained 4 IL-6-dependent lines. Group I 1 contained 2 IL-6-independent lines (one v-abl expressor) that grew faster in the presence of IL-6.
Group 111 consisted of 3 feeder-dependent lines (one v-abl expressor) that were not significantly stimulated by IL-6. These findings indicate that v-abl expression does not influence 11-6 dependence or responsiveness by itself. The supernatant of one line in group I 1 was able to stimulate PC cells. All 6 lines of Groups I and I1 carried a typical (I 2; 15) translocation, while all 3 lines in group 111 had a variant (6; 15) or (I 5; 16) translocation.