中华病理学杂志
中華病理學雜誌
중화병이학잡지
Chinese Journal of Pathology
2015年
7期
486-489
,共4页
晁臣%来茜%骆涛波%唐高燕%周韧%张伟
晁臣%來茜%駱濤波%唐高燕%週韌%張偉
조신%래천%락도파%당고연%주인%장위
癌,肝细胞性%细胞增殖%细胞运动%细胞凋亡
癌,肝細胞性%細胞增殖%細胞運動%細胞凋亡
암,간세포성%세포증식%세포운동%세포조망
Carcinoma,hepatocellular%Cell proliferation%Cell movement%Apoptosis
目的了解人食管癌相关基因4（ ECRG4）在人肝细胞肝癌组织和肝癌细胞系中的表达情况，探讨ECRG4对肝癌细胞增殖、凋亡以及迁移能力的影响。方法提取24例配对肝细胞肝癌组织和癌旁肝组织的总RNA以及正常肝细胞系QSG7701和肝癌细胞系HepG2的总RNA和总蛋白，分别利用即时荧光定量PCR（ RT-qPCR）和Western blot法检测ECRG4的表达；构建ECRG4的真核表达质粒ECRG4-pcDNA3.1，转染肝癌细胞系HepG2，进行体外的细胞增殖、凋亡以及迁移实验。结果与癌旁肝组织相比，在肝细胞肝癌组织中ECRG4 mRNA表达下调或缺失（98.5％，23／24，P＜0.01）；和正常肝细胞系QSG7701相比，ECRG4 mRNA在肝癌细胞系HepG2中的表达明显下调（ P＜0.05）并且其蛋白表达水平也明显降低。转染ECRG4表达质粒后HepG2细胞的增殖和迁移能力明显低于对照组（P＜0.05），细胞凋亡率明显高于对照组（P＜0.05）。结论 ECRG4在肝细胞肝癌中表达下调，在体外肝癌细胞系中过表达ECRG4可抑制细胞的增殖和迁移，促进细胞凋亡，ECRG4可能是肝细胞肝癌潜在的抑癌基因，有望为肝细胞肝癌分子靶向治疗提供新策略。
目的瞭解人食管癌相關基因4（ ECRG4）在人肝細胞肝癌組織和肝癌細胞繫中的錶達情況，探討ECRG4對肝癌細胞增殖、凋亡以及遷移能力的影響。方法提取24例配對肝細胞肝癌組織和癌徬肝組織的總RNA以及正常肝細胞繫QSG7701和肝癌細胞繫HepG2的總RNA和總蛋白，分彆利用即時熒光定量PCR（ RT-qPCR）和Western blot法檢測ECRG4的錶達；構建ECRG4的真覈錶達質粒ECRG4-pcDNA3.1，轉染肝癌細胞繫HepG2，進行體外的細胞增殖、凋亡以及遷移實驗。結果與癌徬肝組織相比，在肝細胞肝癌組織中ECRG4 mRNA錶達下調或缺失（98.5％，23／24，P＜0.01）；和正常肝細胞繫QSG7701相比，ECRG4 mRNA在肝癌細胞繫HepG2中的錶達明顯下調（ P＜0.05）併且其蛋白錶達水平也明顯降低。轉染ECRG4錶達質粒後HepG2細胞的增殖和遷移能力明顯低于對照組（P＜0.05），細胞凋亡率明顯高于對照組（P＜0.05）。結論 ECRG4在肝細胞肝癌中錶達下調，在體外肝癌細胞繫中過錶達ECRG4可抑製細胞的增殖和遷移，促進細胞凋亡，ECRG4可能是肝細胞肝癌潛在的抑癌基因，有望為肝細胞肝癌分子靶嚮治療提供新策略。
목적료해인식관암상관기인4（ ECRG4）재인간세포간암조직화간암세포계중적표체정황，탐토ECRG4대간암세포증식、조망이급천이능력적영향。방법제취24례배대간세포간암조직화암방간조직적총RNA이급정상간세포계QSG7701화간암세포계HepG2적총RNA화총단백，분별이용즉시형광정량PCR（ RT-qPCR）화Western blot법검측ECRG4적표체；구건ECRG4적진핵표체질립ECRG4-pcDNA3.1，전염간암세포계HepG2，진행체외적세포증식、조망이급천이실험。결과여암방간조직상비，재간세포간암조직중ECRG4 mRNA표체하조혹결실（98.5％，23／24，P＜0.01）；화정상간세포계QSG7701상비，ECRG4 mRNA재간암세포계HepG2중적표체명현하조（ P＜0.05）병차기단백표체수평야명현강저。전염ECRG4표체질립후HepG2세포적증식화천이능력명현저우대조조（P＜0.05），세포조망솔명현고우대조조（P＜0.05）。결론 ECRG4재간세포간암중표체하조，재체외간암세포계중과표체ECRG4가억제세포적증식화천이，촉진세포조망，ECRG4가능시간세포간암잠재적억암기인，유망위간세포간암분자파향치료제공신책략。
Objective To investigate the expression of esophageal cancer related gene 4( ECRG4) in human hepatocellular carcinoma and the role of ECRG 4 in proliferation, apoptosis and migration of hepatoma cells .Methods ECRG4 expression was investigated in normal or tumor liver cell lines including QSG7701 and HepG2 cells, and in 24 pairs of fresh samples of hepatocellular carcinoma by quantitative real-time PCR or Western blot.ECRG4-pcDNA3.1 expressing plasmid was transfected into HepG 2 cells, of which cellular proliferation , apoptosis and migration were documented .Results ECRG4 mRNA expression was reduced or absent in most primary hepatocellular carcinoma samples ( 95.8%, 23 out of 24 hepatocellular carcinoma samples ) compared to their paired normal liver samples ( P <0.01 ) .ECRG4 mRNA was significantly lower in HepG2 cells than QSG7701 cells (P<0.05) along with decreased ECRG4 protein expression.HepG2 cells overexpressing ECRG 4 showed decreased proliferation , increased apoptosis and reduced migration as compared with control cells ( P <0.05 ) .Conclusions ECRG4 expression is frequently down-regulated in hepatocellular carcinoma.Overexpression of ECRG 4 inhibits the proliferation and migration but promotes apoptosis of HepG 2 cells,suggesting that ECRG4 is a candidate tumor suppressor gene in hepatocellular carcinoma and therefore may serve as a novel target for precision therapy .
