| Disease | TRYOSINE KINASE ACTIVATION IN MEDIATING THE MITOGENIC ACTION OF PRODACTIN (PRL) HAS BEEN EVALUATED. USE WAS MEDE 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-SFJCDL GENISTEIN WAS A POTENT GROWTH-INHIBITOR FOR BOTH LINES, INHIBITING 2H-THYMIDINE INCORPORATION IN NB2-11 AND NB2-SFJCD1 CELLS WITH IC OF 4.2 AND 6.7 MG/ML RESP. 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 ADDN. WITHIN MINUTES. GENISTEIN INHIBITION OF DNA SYNTHESIS IN G1 ARRESTED NB2-11 CELLS WAS MOST PRONOUNCED IF THE AGEN
WAS ADDED WITHIN 1 B OF PRL TREATMENT. THE RESULTS INDICATE THAT, WHILE BOTH NB2 CELL LINES HAVE A GENERAL GROWTH REQUIREMENT FOR TYROSYL PHOSPHORYLATION, THE EARLY, PRL-INDCUED TYROSINE KINASE ACTIVATION IS A COMPONENT OF THE PRL MITOGENIC
SIGNAL TRANSDUCTIONM PATHWAY. |