中华肝脏外科手术学电子杂志
中華肝髒外科手術學電子雜誌
중화간장외과수술학전자잡지
CHINESE JOURNAL OF HEPATIC SURGERY(ELECTRONIC EDITION)
2014年
4期
247-251
,共5页
唐云强%何璐%唐辉%张琼%洪健
唐雲彊%何璐%唐輝%張瓊%洪健
당운강%하로%당휘%장경%홍건
癌,肝细胞%细胞周期检测点激酶%肿瘤转移
癌,肝細胞%細胞週期檢測點激酶%腫瘤轉移
암,간세포%세포주기검측점격매%종류전이
Carcinoma,hepatocellular%Cell cycle checkpoint kinase%Neoplasm metastasis
目的：探讨细胞周期检测点激酶1（Chk1）在肝细胞癌（肝癌）中的表达及其对肝癌侵袭能力的影响。方法标本来源于2005年6月至2010年6月在广州医科大学附属肿瘤医院行根治性肝切除术的127例患者的肝癌及癌旁组织。所有患者均签署知情同意书，符合医学伦理学规定。其中男116例，女11例；年龄23～77岁，中位年龄50岁。采用免疫组织化学方法检测肝癌和癌旁组织中Chk1表达，并分别采用Huh7和MHCC-97H肝癌细胞进行Transwell细胞侵袭实验。实验分为两组，Chk1抑制剂组（抑制组）加入Chk1小分子抑制剂G?6976，对照组加入0.1%二甲基亚砜（DMSO）。观察肝癌和癌旁组织中Chk1的表达情况，以及Chk1表达与临床病理学参数的关系。两组穿膜细胞数比较采用t检验，率的比较采用χ2检验。结果肝癌组织Chk1阳性率为80.3%（102/127），明显高于癌旁肝组织的15.0%（19/127）（χ2=108.700，P<0.05）。肿瘤数目多发、无肿瘤包膜、术后早期复发的患者肝癌组织中Chk1高表达（χ2=6.289，4.713，5.039；P<0.05）。抑制剂组Huh7和MHCC-97H肝癌细胞的穿膜细胞数分别为（127±8）、（136±10）个，对照组相应为（174±11）、（188±13）个，抑制组明显低于对照组（t=-3.402，-3.136；P<0.05）。结论肝癌组织中存在Chk1高表达，Chk1高表达与肝癌的侵袭和转移有关，Chk1抑制剂可有效抑制肝癌细胞的侵袭能力。
目的：探討細胞週期檢測點激酶1（Chk1）在肝細胞癌（肝癌）中的錶達及其對肝癌侵襲能力的影響。方法標本來源于2005年6月至2010年6月在廣州醫科大學附屬腫瘤醫院行根治性肝切除術的127例患者的肝癌及癌徬組織。所有患者均籤署知情同意書，符閤醫學倫理學規定。其中男116例，女11例；年齡23～77歲，中位年齡50歲。採用免疫組織化學方法檢測肝癌和癌徬組織中Chk1錶達，併分彆採用Huh7和MHCC-97H肝癌細胞進行Transwell細胞侵襲實驗。實驗分為兩組，Chk1抑製劑組（抑製組）加入Chk1小分子抑製劑G?6976，對照組加入0.1%二甲基亞砜（DMSO）。觀察肝癌和癌徬組織中Chk1的錶達情況，以及Chk1錶達與臨床病理學參數的關繫。兩組穿膜細胞數比較採用t檢驗，率的比較採用χ2檢驗。結果肝癌組織Chk1暘性率為80.3%（102/127），明顯高于癌徬肝組織的15.0%（19/127）（χ2=108.700，P<0.05）。腫瘤數目多髮、無腫瘤包膜、術後早期複髮的患者肝癌組織中Chk1高錶達（χ2=6.289，4.713，5.039；P<0.05）。抑製劑組Huh7和MHCC-97H肝癌細胞的穿膜細胞數分彆為（127±8）、（136±10）箇，對照組相應為（174±11）、（188±13）箇，抑製組明顯低于對照組（t=-3.402，-3.136；P<0.05）。結論肝癌組織中存在Chk1高錶達，Chk1高錶達與肝癌的侵襲和轉移有關，Chk1抑製劑可有效抑製肝癌細胞的侵襲能力。
목적：탐토세포주기검측점격매1（Chk1）재간세포암（간암）중적표체급기대간암침습능력적영향。방법표본래원우2005년6월지2010년6월재엄주의과대학부속종류의원행근치성간절제술적127례환자적간암급암방조직。소유환자균첨서지정동의서，부합의학윤리학규정。기중남116례，녀11례；년령23～77세，중위년령50세。채용면역조직화학방법검측간암화암방조직중Chk1표체，병분별채용Huh7화MHCC-97H간암세포진행Transwell세포침습실험。실험분위량조，Chk1억제제조（억제조）가입Chk1소분자억제제G?6976，대조조가입0.1%이갑기아풍（DMSO）。관찰간암화암방조직중Chk1적표체정황，이급Chk1표체여림상병이학삼수적관계。량조천막세포수비교채용t검험，솔적비교채용χ2검험。결과간암조직Chk1양성솔위80.3%（102/127），명현고우암방간조직적15.0%（19/127）（χ2=108.700，P<0.05）。종류수목다발、무종류포막、술후조기복발적환자간암조직중Chk1고표체（χ2=6.289，4.713，5.039；P<0.05）。억제제조Huh7화MHCC-97H간암세포적천막세포수분별위（127±8）、（136±10）개，대조조상응위（174±11）、（188±13）개，억제조명현저우대조조（t=-3.402，-3.136；P<0.05）。결론간암조직중존재Chk1고표체，Chk1고표체여간암적침습화전이유관，Chk1억제제가유효억제간암세포적침습능력。
Objective To investigate the expression of cell cycle checkpoint kinase 1 (Chk1) and its impact on the invasion capacity of hepatocellular carcinoma (HCC). Methods Samples of HCC tissues and adjacent non-tumor tissues from 127 patients undergoing radical hepatectomy in Cancer Center of Guangzhou Medical University from June 2005 to June 2010 were collected. The informed consents of all patients were obtained and the ethical committee approval was received. The patients included 116 males and 11 females with age ranging from 23 to 77 years old and a median age of 50 years old. The expression of Chk1 was detected by immunohistochemistry, and Transwell cell invasion assay was performed using HCC cells Huh7 and MHCC-97H. The experiment was divided into two groups. Chk1 small-molecule inhibitor G?6976 was added in Chk1 inhibitor group (inhibitor group). Dimethyl sulfoxide (DMSO, 0.1%) was added in control group. The expression of Chk1 in HCC tissues and adjacent non-tumor tissues, the relation between Chk1 expression and clinicopathological indicators were observed. The difference of cell-membrane penetrating count in two groups was compared using t test. The comparison of rates was conducted using Chi-square test. Results The positive rate of Chk1 in HCC tissues [80.3%(102/127)] was signiifcantly higher than that in adjacent non-tumor tissues [15.0%(19/127)] (χ2=108.700, P<0.05). High expression of Chk1 was observed in HCC tissues of patients with multiple tumors, non-coating tumors or early tumor recurrence after operation (χ2=6.289, 4.713, 5.039;P<0.05). The cell-membrane penetrating counts of HCC cells Huh7 and MHCC-97H in inhibitor group (127±8, 136±10) were signiifcantly lower than those in control group (174±11, 188±13) ( t=-3.402,-3.136;P<0.05). Conclusions High expression of Chk1 can be observed in HCC tissues. It’s associated with the invasion and metastasis of HCC. The Chk1 inhibitor can effectively suppress the invasion capacity of HCC cells.
