Oncostatin M (OM) promotes the growth of DU 145 human prostate cancer cells, but not PC-3 or LNCaP, through the signaling of the OM specific receptor

Background: Oncostatin M (OM) is a member of the interleukin-6 (IL-6) cytok ine family and all members utilize gp130 as a common signal transducing rec eptor. Tyrosine phosphorylation of the transcription factor STAT3 plays an important role in IL-6 cytokine family-mediated reactions. OM signals are t ransduced through two different OM receptor complexes: a leukemic inhibitor y factor (LIF)/OM receptor (a heterodimer of LIFR beta and gp130) and an OM specific receptor (a heterodimer of OMR beta and gp130); This study examin ed the expression of these two OM receptors as well as the effect of OM on the growth of prostate carcinoma cell lines. Material and Methods: PC-3, DU 145 and LNCaP cells were used The expression of OMR beta and LIFR beta was determined by RT-PCR. Tyrosine phosphorylation of STAT3 was analyzed by We stern blotting. Results: OM promoted the growth of DU 145 but not that of P C-3 and LNCaP LIF had no effect on the growth of any of these cell lines. D U 145 and PC-3 expressed much higher levels of OMR beta mRNA than those of LIFR beta mRNA. Neither OMR beta nor LIFR beta mRNA was detected in LNCaP. OM, but not LIF, induced rapid tyrosine phosphorylation of STAT3 In DU 145. PC-3 lacked STAT3 expression. Conclusions: OM has been known to be a cytos tatic cytokine for tumor cells. Conversely, we show that OM promotes the gr owth of DU 145. Further, our findings suggest that the growth-promoting sig nal of OM is mediated through the OM specific receptor with subsequent acti vation of STAT3.