中华普通外科学文献（电子版）
中華普通外科學文獻（電子版）
중화보통외과학문헌（전자판）
Chinese Archives of General Surgery(Electronic Edition)
2015年
6期
431-436
,共6页
周嘉嘉%陈汝福%邓小耿%高文超%郑上游%程帝%周泉波%张杰
週嘉嘉%陳汝福%鄧小耿%高文超%鄭上遊%程帝%週泉波%張傑
주가가%진여복%산소경%고문초%정상유%정제%주천파%장걸
病毒核心蛋白质类%肝肿瘤%肝炎%丙型%stat3%上皮间质转化
病毒覈心蛋白質類%肝腫瘤%肝炎%丙型%stat3%上皮間質轉化
병독핵심단백질류%간종류%간염%병형%stat3%상피간질전화
Viral core proteins%Liver neoplasms%Hepatitis C%stat3%Epithelial-mesenchymal transition
目的 探讨丙型肝炎病毒核心蛋白(HCVc)对肝癌细胞信号转导子和转录激活子3(stat3)通路及上皮间质转化(EMT)的影响.方法 将含HCVc基因序列的重组质粒pEGFP-N3-HCVc转染人肝癌细胞HepG2,Real-Time PCR和Western blotting检测HCVc、总stat3、磷酸化stat3(p-stat3)及EMT指标蛋白E-cadherin、Vimentin、Snail的表达,划痕实验及Transwell实验检测细胞迁移和侵袭情况.结果 划痕实验及Transwell实验结果显示,过表达HCVc可增强HepG2细胞的迁移和侵袭能力;stat3通路抑制剂AG490处理可抑制HepG2细胞的侵袭能力.RT-PCR和Western blotting结果显示,过表达HCVc后,HepG2细胞中p-stat3、Vimentin及Snail在表达升高, E-cadherin表达下降;AG490处理可下调p-stat3、Vimentin及Snail表达,增强E-cadherin表达.结论 HCVc可活化stat3通路促进肝癌细胞上皮间质转化,增强肝癌细胞的迁移和侵袭能力.
目的 探討丙型肝炎病毒覈心蛋白(HCVc)對肝癌細胞信號轉導子和轉錄激活子3(stat3)通路及上皮間質轉化(EMT)的影響.方法 將含HCVc基因序列的重組質粒pEGFP-N3-HCVc轉染人肝癌細胞HepG2,Real-Time PCR和Western blotting檢測HCVc、總stat3、燐痠化stat3(p-stat3)及EMT指標蛋白E-cadherin、Vimentin、Snail的錶達,劃痕實驗及Transwell實驗檢測細胞遷移和侵襲情況.結果 劃痕實驗及Transwell實驗結果顯示,過錶達HCVc可增彊HepG2細胞的遷移和侵襲能力;stat3通路抑製劑AG490處理可抑製HepG2細胞的侵襲能力.RT-PCR和Western blotting結果顯示,過錶達HCVc後,HepG2細胞中p-stat3、Vimentin及Snail在錶達升高, E-cadherin錶達下降;AG490處理可下調p-stat3、Vimentin及Snail錶達,增彊E-cadherin錶達.結論 HCVc可活化stat3通路促進肝癌細胞上皮間質轉化,增彊肝癌細胞的遷移和侵襲能力.
목적 탐토병형간염병독핵심단백(HCVc)대간암세포신호전도자화전록격활자3(stat3)통로급상피간질전화(EMT)적영향.방법 장함HCVc기인서렬적중조질립pEGFP-N3-HCVc전염인간암세포HepG2,Real-Time PCR화Western blotting검측HCVc、총stat3、린산화stat3(p-stat3)급EMT지표단백E-cadherin、Vimentin、Snail적표체,화흔실험급Transwell실험검측세포천이화침습정황.결과 화흔실험급Transwell실험결과현시,과표체HCVc가증강HepG2세포적천이화침습능력;stat3통로억제제AG490처리가억제HepG2세포적침습능력.RT-PCR화Western blotting결과현시,과표체HCVc후,HepG2세포중p-stat3、Vimentin급Snail재표체승고, E-cadherin표체하강;AG490처리가하조p-stat3、Vimentin급Snail표체,증강E-cadherin표체.결론 HCVc가활화stat3통로촉진간암세포상피간질전화,증강간암세포적천이화침습능력.
Objective To investigate the role of hepatitis C virus core protein (HCVc) on the ac-tivation of stat3 pathway and regulation of epithelial-mesenchymal transition in hepatocellular cells, which might be involved in tumor metastasis of liver cancer. Methods Recombinant plasmid pEGFP-N3-HCVc containing HCVc gene was transfected to over-expressed HCVc in HepG2 cells. Real-Time PCR and Western blotting were used to detect the expression of HCVc, stat3, phosphorylated stat3 (p-stat3), E-cadherin, Vimentin and Snail. Wound healing test and Transwell assay was employed to de-tect cell migration and invasiveness. Results Wound healing test and Transwell assay showed that over-expression of HCVc in HepG2 cells promoted the cell migration and invasiveness. Meanwhile, AG490 treatment inhibited cell migration and invasiveness of HCVc over-expressing cells. RT-PCR and Western blotting analysis showed that expression of HCVc, p-stat3, Vimentin and Snail were increased and E-cad-herin was decreased in HCVc over-expressing HepG2 cells. Treatment of AG490 on HCVc over-express-ing cells could attenuate HCVc-induced up-regulation of p-stat3, Vimentin and Snail expression and down-regulation of E-cadherin. Conclusion HCVc activates stat3 pathway and promotes epithelial-mesenchymal transition in HepG2 cells, which may be associated with enhanced cell migration and inva-sion in liver cancer.
