Abstract

Objective To observe the impact of growth hormone (GH) on expression of phosphoJAK2 (pJAK2) in pancreatic carcinoma cells and to discuss significance of pJAK2 in signaling.Methods (1)Pancreatic carcinoma cells (SW-1990,Cap-1,ASPC) during exponential growth stage were harvested and cultured in medium containing growth hormone(50 μg/L,100μg/L);After 24,48,72 hours,cells were counted using a Coulter Counter.(2)Athymic nude BALB/C mice were inoculated with SW-1990 cells,When tumors became palpable after inoculation.animals were randomized to receive GH(4 mg/kg.s.c.once daily for 2 weeks,n=21)versus saline control cytotoxic lymphocyte(CTL,n=7).(3)Human pancreatic carcinoma cell lines(SW-1990,Cap-1,Colo,Mia,Aspc,P3,Panc-1) were collected to detect the basal expression of pJAK2 with immol/lunoblots;After GH administration on special times(in vitro:5,10,15,30,45 min,1,2 h;in vivo:1,2,24 h),Cells were collected and Tumor tissues of the mice were rapidly incised respectively.All the specimen were frozen immol/lediately for subsequent Western blotting analysis,to ohserve the impact of GH on expression of pJAK2 in SW-1990 and inoculation tumor cells.Results The results revealed GH stimulated cell growth in vitro;On immol/lunoblots,positive expression of pJAK2 was observed on human pancreatic carcinoma cell lines(SW-1990、Cap-1、Colo、Mia、Aspc、P3、Panc-1).GH augmented rapidly tyrosine phosphorylation of this special proteins to the highest value on the 5th minute after GH administration in vitro and the values fluctuated later;No similar phenomena,however,were observed in vivo.Conclusion Positive expression of pJAK2 is observed on human pancreatic cancer ceils;Furthermore,GH augments rapidly tyrosine phosphorylation of these special proteins not in vivo but in vitro;and this discrepancy helps to explain why GH doesn't accelerate tumor growth in vivo. Key words: Growth hormone; Pancreatic carcinoma; pJAK2

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