肿瘤研究与临床
腫瘤研究與臨床
종류연구여림상
CANCER RESEARCH AND CLINIC
2009年
12期
826-829
,共4页
胆管肿瘤%TNF相关凋亡诱导配体%半胱氨酸天冬氨酸蛋白酶3%NF-κB
膽管腫瘤%TNF相關凋亡誘導配體%半胱氨痠天鼕氨痠蛋白酶3%NF-κB
담관종류%TNF상관조망유도배체%반광안산천동안산단백매3%NF-κB
Bile duct neoplasms%TNF-related apoptosis-inducing ligand%Caspase-3%NF-kappa B
目的 探讨TRAIL、Caspase-3及NF-κB在胆管癌发生、发展及侵袭中的作用.方法 运用原位杂交、免疫组织化学法检测TRAIL、Caspase-3及NF-κB在胆管癌中的表达情况.结果 TRAIL在胆管癌及癌旁正常胆管组织中的阳性表达率分别为45.2%(19/42)、53.3%(8/15),差异无统计学意义(P>0.05);其在胆管癌的不同临床、病理特征之间的表达差异亦无统计学意义(P均>0.05).Caspase-3在胆管癌组织中的阳性表达率为30.9%(13/42),明显低于癌旁正常胆管组织中的60.0%(9/15)(P<0.05):NF-κB在胆管癌组织中的阳性表达率为61.9%(26/42),明显高于癌旁正常胆管组织中的26.7%(4/15)(P<0.05).胆管癌中Caspase-3、NF-κB的表达均与患者的性别、年龄、病变部位无关(P>0.05),而与是否转移扩散、组织分化程度及生存时间有关(P<0.05).此外,胆管癌中TRAIL表达与Caspase-3的表达呈正相关(P<0.05),NF-κB与Caspase-3呈负相关(P<0.05),TRAIL与NF-κB无相关性(P>0.05).结论 TRAIL表达无肿瘤特异性,表达水平的高低并不能完全决定胆管癌转移扩散与否,亦不能完全决定其恶性程度和预后.NF-κB的活化、Caspase-3的失活或缺失可能促进了肿瘤的转移扩散,并导致了不良的预后.NF-κB通过抑制Caspase-3的活性,从而阻断了TRAIL介导的凋亡途径,使得组织逃避凋亡而无限增生,导致了肿瘤的发生、发展及转移扩散.
目的 探討TRAIL、Caspase-3及NF-κB在膽管癌髮生、髮展及侵襲中的作用.方法 運用原位雜交、免疫組織化學法檢測TRAIL、Caspase-3及NF-κB在膽管癌中的錶達情況.結果 TRAIL在膽管癌及癌徬正常膽管組織中的暘性錶達率分彆為45.2%(19/42)、53.3%(8/15),差異無統計學意義(P>0.05);其在膽管癌的不同臨床、病理特徵之間的錶達差異亦無統計學意義(P均>0.05).Caspase-3在膽管癌組織中的暘性錶達率為30.9%(13/42),明顯低于癌徬正常膽管組織中的60.0%(9/15)(P<0.05):NF-κB在膽管癌組織中的暘性錶達率為61.9%(26/42),明顯高于癌徬正常膽管組織中的26.7%(4/15)(P<0.05).膽管癌中Caspase-3、NF-κB的錶達均與患者的性彆、年齡、病變部位無關(P>0.05),而與是否轉移擴散、組織分化程度及生存時間有關(P<0.05).此外,膽管癌中TRAIL錶達與Caspase-3的錶達呈正相關(P<0.05),NF-κB與Caspase-3呈負相關(P<0.05),TRAIL與NF-κB無相關性(P>0.05).結論 TRAIL錶達無腫瘤特異性,錶達水平的高低併不能完全決定膽管癌轉移擴散與否,亦不能完全決定其噁性程度和預後.NF-κB的活化、Caspase-3的失活或缺失可能促進瞭腫瘤的轉移擴散,併導緻瞭不良的預後.NF-κB通過抑製Caspase-3的活性,從而阻斷瞭TRAIL介導的凋亡途徑,使得組織逃避凋亡而無限增生,導緻瞭腫瘤的髮生、髮展及轉移擴散.
목적 탐토TRAIL、Caspase-3급NF-κB재담관암발생、발전급침습중적작용.방법 운용원위잡교、면역조직화학법검측TRAIL、Caspase-3급NF-κB재담관암중적표체정황.결과 TRAIL재담관암급암방정상담관조직중적양성표체솔분별위45.2%(19/42)、53.3%(8/15),차이무통계학의의(P>0.05);기재담관암적불동림상、병리특정지간적표체차이역무통계학의의(P균>0.05).Caspase-3재담관암조직중적양성표체솔위30.9%(13/42),명현저우암방정상담관조직중적60.0%(9/15)(P<0.05):NF-κB재담관암조직중적양성표체솔위61.9%(26/42),명현고우암방정상담관조직중적26.7%(4/15)(P<0.05).담관암중Caspase-3、NF-κB적표체균여환자적성별、년령、병변부위무관(P>0.05),이여시부전이확산、조직분화정도급생존시간유관(P<0.05).차외,담관암중TRAIL표체여Caspase-3적표체정정상관(P<0.05),NF-κB여Caspase-3정부상관(P<0.05),TRAIL여NF-κB무상관성(P>0.05).결론 TRAIL표체무종류특이성,표체수평적고저병불능완전결정담관암전이확산여부,역불능완전결정기악성정도화예후.NF-κB적활화、Caspase-3적실활혹결실가능촉진료종류적전이확산,병도치료불량적예후.NF-κB통과억제Caspase-3적활성,종이조단료TRAIL개도적조망도경,사득조직도피조망이무한증생,도치료종류적발생、발전급전이확산.
Objective To investigate the function of TRAIUCaspase-3 and NF-κB among the occurrence, development and malignant invasion of bile duct carcinoma. Methods The in-situ hybrization technique and immunochemistry method were adopted to detect expression of TRAIL, Caspase-3 and NF-κB. Results The positive rates of TRAIL expression in carcinoma of bile duct and paracancer tissue were 45.2 % (19/42) and 53.3 %(8/15), respectively. The differences were not significant (P >0.05), and there were no evident difference between expression of TRAIL and every clinic pathology factor(P >0.05). The positive rates of Caspase-3 expression in carcinoma of bile duct were 30.9 %(13/42), which were obviously lower than those in paracancer tissue, 60.0 %(9/15)(P<0.05). However, The positive rates of NF-κB expression in carcinoma of bile duct were 61.9 %(26/42), obviously higher than those in paracancer tissue, 26.7 %(4/15)(P <0.05). The positive rates of Caspase-3, NF-κB expression were relation to metastasis and proliferation, differentiation degree of tissue and survival time (P <0.05), but were independent of sex, ages and position of carcinoma(P > 0.05). Moreover, TRAIL and Caspase-3 manifested positive relationship (P <0.05). On the contrary , NF-κB and Caspase-3 manifested negative relationship (P <0.05). However, there was no relationship between TRAIL and NF-κB(P >0.05). Conclusion Expression of TRAIL has no selectivity of tumour, Its expression is higher or lower which couldn' t absolutely decide tumour' s metastasis and proliferation, and could not decide malignant degree and prognosis of tumour, too. Activation of NF-κB and losing action or absence of Caspase-3 possibly accelerate metastasis and proliferation of tumour, which result in bad prognosis. NF-κB interdicte TRAIL inducing apoptosis approach via control activation of NF-κB, which induce tissue to avoiding apoptosis and multiplication unboundedly, leading to tumour's occurrence, development, metastasis and diffuseness.
