安徽医科大学学报
安徽醫科大學學報
안휘의과대학학보
ACTA UNIVERSITY MEDICINALIS ANHUI
2014年
6期
795-799
,共5页
陈静%李建生%刘文斌%荚卫东%许戈良%马金良%余继海%葛勇胜
陳靜%李建生%劉文斌%莢衛東%許戈良%馬金良%餘繼海%葛勇勝
진정%리건생%류문빈%협위동%허과량%마금량%여계해%갈용성
肝肿瘤%Mortalin%血管生成%上皮间质转化
肝腫瘤%Mortalin%血管生成%上皮間質轉化
간종류%Mortalin%혈관생성%상피간질전화
liver neoplasms%Mortalin%angiogenesis%EMT
目的:检测热休克蛋白75( Mortalin)在肝细胞癌中的表达,探讨其与血管生成和上皮间质转化( EMT)的关系。方法收集100例原发性肝癌( HCC)患者的癌组织和癌旁组织及10例正常肝组织,采用免疫组织化学染色、Western blot和qPCR检测Mortalin的表达,分析Mortalin表达与肝癌临床病理特征之间的关系。同时分析100例HCC患者癌组织中Mortalin、波形蛋白( Vimentin)和微血管密度( MVD)的表达情况,判断Mortalin的表达与EMT、肿瘤血管生成之间的关系。结果免疫组织化学显示Mortalin主要表达在细胞质中。肝癌组织中高表达Mortalin的比率是77%,显著高于癌旁组织的19%和正常组织的10%(χ2=67.388,16.669;P<0.01)。 Mortalin的高表达与肝癌Edmondson分级、TNM分期、血管侵犯和淋巴结转移有关(P<0.05)。 Western blot和qPCR检测结果显示肝癌组织中Mortalin相对含量明显高于癌旁和正常组织( P<0.05)。免疫组织化学染色检查显示,肝癌组织中Mortalin的表达与Vimentin的表达存在正相关(r=0.235, P<0.05),而高表达Mortalin的肝癌组织比低表达的有更高的MVD的趋势,但差异无统计学意义( t=1.630, P>0.05)。结论 Mortalin不能促进肝癌血管形成,但可能通过诱导肝癌组织的 EMT而参与肝癌的侵袭和转移。
目的:檢測熱休剋蛋白75( Mortalin)在肝細胞癌中的錶達,探討其與血管生成和上皮間質轉化( EMT)的關繫。方法收集100例原髮性肝癌( HCC)患者的癌組織和癌徬組織及10例正常肝組織,採用免疫組織化學染色、Western blot和qPCR檢測Mortalin的錶達,分析Mortalin錶達與肝癌臨床病理特徵之間的關繫。同時分析100例HCC患者癌組織中Mortalin、波形蛋白( Vimentin)和微血管密度( MVD)的錶達情況,判斷Mortalin的錶達與EMT、腫瘤血管生成之間的關繫。結果免疫組織化學顯示Mortalin主要錶達在細胞質中。肝癌組織中高錶達Mortalin的比率是77%,顯著高于癌徬組織的19%和正常組織的10%(χ2=67.388,16.669;P<0.01)。 Mortalin的高錶達與肝癌Edmondson分級、TNM分期、血管侵犯和淋巴結轉移有關(P<0.05)。 Western blot和qPCR檢測結果顯示肝癌組織中Mortalin相對含量明顯高于癌徬和正常組織( P<0.05)。免疫組織化學染色檢查顯示,肝癌組織中Mortalin的錶達與Vimentin的錶達存在正相關(r=0.235, P<0.05),而高錶達Mortalin的肝癌組織比低錶達的有更高的MVD的趨勢,但差異無統計學意義( t=1.630, P>0.05)。結論 Mortalin不能促進肝癌血管形成,但可能通過誘導肝癌組織的 EMT而參與肝癌的侵襲和轉移。
목적:검측열휴극단백75( Mortalin)재간세포암중적표체,탐토기여혈관생성화상피간질전화( EMT)적관계。방법수집100례원발성간암( HCC)환자적암조직화암방조직급10례정상간조직,채용면역조직화학염색、Western blot화qPCR검측Mortalin적표체,분석Mortalin표체여간암림상병리특정지간적관계。동시분석100례HCC환자암조직중Mortalin、파형단백( Vimentin)화미혈관밀도( MVD)적표체정황,판단Mortalin적표체여EMT、종류혈관생성지간적관계。결과면역조직화학현시Mortalin주요표체재세포질중。간암조직중고표체Mortalin적비솔시77%,현저고우암방조직적19%화정상조직적10%(χ2=67.388,16.669;P<0.01)。 Mortalin적고표체여간암Edmondson분급、TNM분기、혈관침범화림파결전이유관(P<0.05)。 Western blot화qPCR검측결과현시간암조직중Mortalin상대함량명현고우암방화정상조직( P<0.05)。면역조직화학염색검사현시,간암조직중Mortalin적표체여Vimentin적표체존재정상관(r=0.235, P<0.05),이고표체Mortalin적간암조직비저표체적유경고적MVD적추세,단차이무통계학의의( t=1.630, P>0.05)。결론 Mortalin불능촉진간암혈관형성,단가능통과유도간암조직적 EMT이삼여간암적침습화전이。
Objective To detect the expression of Heat shock protein 75 ( Mortalin ) in hepatocellular carcinoma ( HCC) ,and explore its relationship with angiogenesis and epithelial-mesenchymal transition ( EMT) . Methods A hundred cases of HCC tumor and paracarcinomatous tissues, and ten cases of normal liver tissues were collected. The expression of Mortalin and relationship between Mortalin and clinicopathological characteristics of HCC were detected and analyzed using immunohistochemistry, Western blot and qPCR. The expressions of Mortalin, Vimen-tin and microvessel density ( MVD) in 100 HCC tumor tissues were detected by immunohistochemistry, and then the relationship was judged between the expression of Mortalin, EMT and angiogenesis. Results Immunohisto-chemistry showed that Mortalin mainly expressed in the cytoplasm. The high expression rate of Mortalin in HCC tumor tissues was 77%, which was remarkably higher than that in paracarcinomatous tissues ( 19%) and normal liver tissues ( 10%) (χ2 =67. 388 , 16. 669;P<0. 01 ) . The high expression of Mortalin in HCC was correlated with Edmondson grade, TNM stage, vascular invasion and lymph node metastasis ( P<0. 05 ) . Western blot and qPCR analysis showed that relative content of Mortalin in HCC was significantly higher than that in paracarcinoma-tous and normal tissues ( P<0. 05 ) . A significant positive correlation was found between the expression of Mortalin and Vimentin ( r=0. 235 , P<0. 05 ) , but the high expression of Mortalin group had a tendency to higher MVD than that in low expression of Mortalin group ( t=1. 630 , P>0. 05 ) . Conclusion The high expression of Mortalin can not promote angiogenesis, but may accelerate invasion and metastasis of HCC through inducing EMT.