论文部分内容阅读
AIM:To investigate the potential involvement of leptin incarcinogenesis of hepatocellular carcinoma(HCC)and toelucidate the etiology,carcinogenesis and progress of HCC.METHODS:Expressions of Ob gene product,leptin and itsreceptor,Ob-R were investigated in 36 cases of HCC specimensand corresponding adjacent non-tumorous liver tissues withimmunohistochemical staining.The effect of leptin onproliferation of Chang liver cell line and liver cancer cell lineSMMC-7721 was studied with cell proliferation assay(MTT),RESULTS:Leptin expression was detected in 36 cases ofadjacent non-tumorous liver tissues(36/36,100%)withmoderate(++)to strong(+++)intensity;and in 72.22%(26/36)of HCC with weaker(+)intensity(P<0.05).Thirtyof 36(83.33%)cases of adjacent non-tumorous livertissues were positive for Ob-R,with moderate(++)tostrong(+++)intensity.In HCC,11/36(30.56%)cases werepositive,with weak(+)intensity(P<0.05).In cellproliferation assay,leptin inhibited the proliferation of Changliver cells.The cell survival rate was 10-13% lower thanthat of the untreated cells(P>0.05).Leptin had little effecton the proliferation of liver cancer cells(P>0.05).CONCLUSION:High level expression and decreased orabsent expression of leptin and its receptor in adjacentnon-tumorous liver cells and HCC cells,inhibitory effect ofleptin on the proliferation of normal Chang liver cells andno effect of leptin on proliferation of liver cancer cells,may provide new insights into the carcinogenesis andprogression of human HCC.It could be assumed that leptinacting as an inhibitor and/or promoter,is involved in theprocess of carcinogenesis and progress of human HCC.
AIM: To investigate the potential involvement of leptin incarcinogenesis of hepatocellular carcinoma (HCC) and toelucidate the etiology, carcinogenesis and progress of HCC. METHODS: Expressions of Ob gene product, leptin and its receptor, Ob-R were investigated in 36 cases of HCC specimensand corresponding adjacent non-tumorous liver tissues with immunohistochemical staining. The effect of leptin onproliferation of Chang liver cell line and liver cancer cell line SMMC-7721 was studied with cell proliferation assay (MTT), RESULTS: Leptin expression was detected in 36 cases of adjacent non-tumorous The HCC with weaker (+) intensity (36/36, 100%) withmoderate (++) to strong (+++) intensity; and in 72.22% (26/36) ) cases of adjacent non-tumorous livertissues were positive for Ob-R, with moderate (++) tostrong (+++) intensity.In HCC, 11/36 (30.56%) cases werepositive, with weak (+) intensity <0.05) .In cellproliferation assay, leptin inhibited the proliferation of Changliver cells.The cell su rvival rate was 10-13% lower thanthat of the untreated cells (P> 0.05). Leptin had little effect on the proliferation of liver cancer cells (P> 0.05) .CONCLUSION: High level expression and decreased orabsent expression of leptin and its receptor in adjacentnon-tumorous liver cells and HCC cells, inhibitory effect of leptin on the proliferation of normal Chang liver cells and no effect of leptin on proliferation of liver cancer cells, may provide new insights into the carcinogenesis and protression of human HCC. At could be assumed that leptinacting as an inhibitor and / or promoter, is involved in the process of carcinogenesis and progress of human HCC.