CAJ | 학술논문

目的观察STAT3抑制剂对人原发性肝癌细胞增殖的抑制和诱导细胞凋亡.方法对照组为人原发性肝癌细胞株(HepG2、Huh7),实验组为对照组+STAT3抑制剂(Piceatannol),阴性对照组为人宫颈癌细胞株(Hela),阳性对照组为Hela细胞+干扰素(IFN)-α.Western blot测定STAT3蛋白和磷酸化STAT3蛋白在人肝癌细胞中的表达水平,流式细胞仪检测细胞周期和细胞凋亡率.结果 (1)STAT3蛋白和磷酸化STAT3蛋白构成性表达于人肝癌细胞HepG2和Huh7.STAT3抑制剂抑制实验组磷酸化STAT3蛋白的表达.(2)实验组HepG2的S期细胞的比例[24 h,(15.48±4.91)%～(40.24±0.96)%,P<0.05;48 h,(19.16±1.70)%～(25.62±1.41)%,P<0.05]和Huh7的S期细胞的比例[24 h,(8.55±0.69)%～(31.62±0.20)%,P<0.05;48 h,(7.57±0.62)%～(30.88 ±0.04)%,P<0.05]明显低于对照组;实验组HepG2细胞的早期细胞凋亡率明显高于对照组[(4.50±0.76)%～(2.58±0.76)%,P<0.05],实验组Huh7细胞的早期细胞凋亡率[24 h,(8.27±2.47)%～(23.95±4.72)%,P<0.05]和晚期细胞凋亡率[24 h,(11.6±2.39)%～(25.27±3.51)%,P<0.01;48 h,(11.27±0.87)%～(33.9±2.4)%,P<0.05]明显高于对照组.结论 STAT3抑制剂可以通过阻断JAK-STAT3信号通路途径抑制人原发性肝癌细胞的增殖和诱导凋亡.
목적 관찰STAT3억제제대인원발성간암세포증식적억제화유도세포조망.방법 대조조위인원발성간암세포주(HepG2、Huh7),실험조위대조조+STAT3억제제(Piceatannol),음성대조조위인궁경암세포주(Hela),양성대조조위Hela세포+간우소(IFN)-α.Western blot측정STAT3단백화린산화STAT3단백재인간암세포중적표체수평,류식세포의검측세포주기화세포조망솔.결과 (1)STAT3단백화린산화STAT3단백구성성표체우인간암세포HepG2화Huh7.STAT3억제제억제실험조린산화STAT3단백적표체.(2)실험조HepG2적S기세포적비례[24 h,(15.48±4.91)%～(40.24±0.96)%,P<0.05;48 h,(19.16±1.70)%～(25.62±1.41)%,P<0.05]화Huh7적S기세포적비례[24 h,(8.55±0.69)%～(31.62±0.20)%,P<0.05;48 h,(7.57±0.62)%～(30.88 ±0.04)%,P<0.05]명현저우대조조;실험조HepG2세포적조기세포조망솔명현고우대조조[(4.50±0.76)%～(2.58±0.76)%,P<0.05],실험조Huh7세포적조기세포조망솔[24 h,(8.27±2.47)%～(23.95±4.72)%,P<0.05]화만기세포조망솔[24 h,(11.6±2.39)%～(25.27±3.51)%,P<0.01;48 h,(11.27±0.87)%～(33.9±2.4)%,P<0.05]명현고우대조조.결론 STAT3억제제가이통과조단JAK-STAT3신호통로도경억제인원발성간암세포적증식화유도조망.
Objective To study the janus kinase-signal transducer and activator of transcription 3 ( STAT3 ) inhibitor (Piceatannol) on the growth of hepatocellular carcinoma (HCC) in vitro.Methods The present study created four groups: control group,primary human HCC cell lines ( HepG2,Huh7 );study group,control group + Piceatannol; negative control group,human cervical carcinoma cell line (Hela); positive control group,Hela + interferon (IFN) -α.The protein levels of STAT3 and phosphorylated STAT3 were detected by Western blotting.The cell cycle and rate of apoptotic cells were quantified by flow cytometric analysis.Results ( 1 ) The protein of STAT3 and phosphorylated-STAT3 were constitutively activated in HepG2 and Huh7 cells.The Piceatannol could down-regulate the phosphorylated-STAT3 in study group.(2) Compared to control group,the percentage of HepG2 cells in S phase [24 h,(15.48±4.91)%-(40.24±0.96)%,P＜0.05; 48 h,(19.16 ±1.70)%-(25.62 ±1.41)%,P＜0.05]and that of Huh7 cells in S phase [24 h,( 8.55 ± 0.69 ) % -( 31.62 ± 0.20) %,P ＜ 0.05; 48 h,(7.57 ±0.62 ) % - (30.88 ± 0.04) %,P ＜ 0.05]were decreased significantly in study group.The rate of early apoptotic cells in HepG2 [(4.50 ± 0.76 ) % -( 2.58 ± 0.76 ) %,P ＜ 0.05]was increased significantly in study group and that in Huh7 [24 h,(8.27 ±2.47)%-(23.95 ±4.72)% ,P＜0.05],and the rate of late apoptotic cells in Huh7 [24 h,( 11.6 ± 2.39 ) % - ( 25.27 ± 3.51 ) %,P ＜ 0.01; 48 h,( 11.27 ±0.87)%-(33.9 ±2.4)% ,P ＜0.05]increased significantly in study group.Conclusion Through blocking Janus kinase-signal transducer and activator of transcription signaling pathway,Piceatannol could suppress proliferation and induce apoptosis of human HCC cells.