Induction of rcl, a novel growth-related gene by Coptidis Rhizoma in rat H4IIE cells

Exposure of rat hepatoma cells to a low concentration of Coptidis Rhizoma reduces cell viability and probably induces apoptotic cell death. However, Coptidis Rhizoma treatment increased the expression of a putative c-myc-responsive gene rcl and could increase the activity of a transcription factor in inhibiting the growth of cancer cells. This increase was accompanied by an increment in the expression of mRNA for c-myc-responsive gene. The expression was analysed by PCR and confirmed by Northern blot analysis. The rcl expression level increases with the Coptidis Rhizoma concentration, and in the time-course study. The results suggest the expression of rcl is important to the fate of cell growth, since overexpression of the c-myc proto-oncogene cell proliferation, differentiation, and apoptosis can be regulated by the treatment of Coptidis rhizoma. Additionally, difference between overexpression of c-myc-responsive gene in the control suggested that this protein was responsible for the inhibitory effect of a transcriptional factor on cell growth. The results support the notion of rcl as an important antiapoptotic protein mediating sensitivity to Coptidis Rhizoma induction in cancer cells. rcl may play an important role during cellular proliferation and c-myc-mediated transformation. (C) 2002 Elsevier Science Inc. All rights reserved.