The s-Myc protein having the ability to induce apoptosis is selectively expressed in rat embryo chondrocytes
Asai, A.; Miyagi, Y.; Sugiyama, A.; Nagashima, Y.; Kanemitsu, H.; Obinata, M.; Mishima, K.; Kuchino, Y.
Oncogene 9(8): 2345-2352
1994
ISSN/ISBN: 0950-9232 PMID: 8036017 Document Number: 437753
Gene transfection experiments demonstrated that overexpression of the s-myc gene under the control of a human metallothionein promoter induced apoptosis in cells such as rat and human glioma cells. In contrast to c-Myc-mediated apoptosis requiring withdrawal of serum growth factors, s-myc expression induced apoptosis in glioma cells in the presence of 10% fetal calf serum. Whereas, s-Myc-mediated apoptosis was suppressed in proportion to the increase of bcl-2 expression as seen in c-Myc mediated apoptosis. The s-myc gene was expressed in rat embryo cells being committed to differentiate to hypertrophic chondrocytes which undergo programmed cell death. CAT assay demonstrated that in the NH-2-terminal region, the s-Myc protein contains a domain structure required for expression of transactivation activity that is approximately six times higher than that of c-Myc. Therefore, these findings strongly suggest that s-Myc may play an important role in transcription regulation of a set of genes whose expression induces programmed cell death in vitro and in vivo.