Inhibition by genistein of prolactin-induced Nb2 lymphoma cell mitogenesis.
Tyrosine kinase activation in mediating the mitogenic action of prolactin ( PRL) has been evaluated. Use was made of genistein, a tyrosine kinase antagonist, and cultured rat Nb2 lymphoma cells, i.e. the lactogen-dependent Nb2-11 line and a lactogen-independent subline, Nb2-SFJCD1. Genistein was found to be a potent growth-inhibitor for both lines, inhibiting 3H-thymidine incorporation in Nb2-11 and Nb2-SFJCD1 cells with IC50s of 4.2 and 6.7 micrograms/ml, respectively. Genistein also inhibited expression and translation of the heat shock protein 70 gene and pp40 protein substrate phosphorylation which, in Nb2-11 cells, followed PRL addition within minutes. Genistein inhibition of DNA synthesis in G1-arrested Nb2-11 cells was most pronounced if the agent was added within 1 h of PRL treatment. The results indicate that, while both Nb2 cell lines have a general growth requirement for tyrosyl phosphorylation, the early, PRL-induced tyrosine kinase activation is a component of the PRL mitogenic signal transduction pathway.[1]References
- Inhibition by genistein of prolactin-induced Nb2 lymphoma cell mitogenesis. Buckley, A.R., Buckley, D.J., Gout, P.W., Liang, H., Rao, Y.P., Blake, M.J. Mol. Cell. Endocrinol. (1993) [Pubmed]
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