中华消化外科杂志
中華消化外科雜誌
중화소화외과잡지
CHINESE JOURNAL OF DIGESTIVE SURGERY
2009年
5期
360-363
,共4页
茆家定%吴佩%杨应林%武健%黄鹤
茆傢定%吳珮%楊應林%武健%黃鶴
묘가정%오패%양응림%무건%황학
结直肠肿瘤%生长抑素%Fas/FasL%半胱天冬蛋白酶
結直腸腫瘤%生長抑素%Fas/FasL%半胱天鼕蛋白酶
결직장종류%생장억소%Fas/FasL%반광천동단백매
Colorectal neoplasms%Somatostatin%Fas/FasL%Caspase
目的 探讨生长抑素对大肠癌细胞凋亡的影响.方法 采用巢式RT-PCR方法检测2004年1月至2006年10月皖南医学院附属弋矶山医院收治的79例大肠癌患者癌组织中生长抑素mRNA的表达情况,采用免疫组织化学法检测大肠癌组织中生长抑素、Fas、FasL、半胱天冬蛋白酶(caspase)3和8蛋白的表达情况,TUNEL法检测细胞凋亡指数(AI).采用χ~2检验、q检验、Spearman等级相关检验对结果进行分析.结果 大肠癌组织中生长抑素mRNA与其蛋白表达呈正相关(r=0.98,P<0.05).低分化和中分化大肠癌组织中生长抑素mRNA及其蛋白的表达明显低于高分化组织(χ~2=10.78,11.24,5.27,5.24,P<0.05);生长抑素mRNA及其蛋白在乳头状腺癌的阳性表达率明显高于黏液腺癌+印戒细胞癌及未分化癌(χ~2=6.56,6.99,5.44,7.39,P<0.05);Dukes A、B期的生长抑素mRNA及其蛋白阳性表达率明显高于C、D期(χ~2=5.17,4.06,P<0.05).生长抑素高表达组、中表达组的AI明显高于低表达组(q=5.66,4.21,P<0.05);Fas、caspase-8、caspase-3在生长抑素高表达组、中表达组的阳性表达率明显高于低表达组(χ~2=5.48,5.62,6.89,4.32,4.19,3.91,P<0.05).结论 生长抑素对大肠癌细胞凋亡的调控可能与Fas/FasL基因的表达失衡、功能和信号系统的紊乱有关.
目的 探討生長抑素對大腸癌細胞凋亡的影響.方法 採用巢式RT-PCR方法檢測2004年1月至2006年10月皖南醫學院附屬弋磯山醫院收治的79例大腸癌患者癌組織中生長抑素mRNA的錶達情況,採用免疫組織化學法檢測大腸癌組織中生長抑素、Fas、FasL、半胱天鼕蛋白酶(caspase)3和8蛋白的錶達情況,TUNEL法檢測細胞凋亡指數(AI).採用χ~2檢驗、q檢驗、Spearman等級相關檢驗對結果進行分析.結果 大腸癌組織中生長抑素mRNA與其蛋白錶達呈正相關(r=0.98,P<0.05).低分化和中分化大腸癌組織中生長抑素mRNA及其蛋白的錶達明顯低于高分化組織(χ~2=10.78,11.24,5.27,5.24,P<0.05);生長抑素mRNA及其蛋白在乳頭狀腺癌的暘性錶達率明顯高于黏液腺癌+印戒細胞癌及未分化癌(χ~2=6.56,6.99,5.44,7.39,P<0.05);Dukes A、B期的生長抑素mRNA及其蛋白暘性錶達率明顯高于C、D期(χ~2=5.17,4.06,P<0.05).生長抑素高錶達組、中錶達組的AI明顯高于低錶達組(q=5.66,4.21,P<0.05);Fas、caspase-8、caspase-3在生長抑素高錶達組、中錶達組的暘性錶達率明顯高于低錶達組(χ~2=5.48,5.62,6.89,4.32,4.19,3.91,P<0.05).結論 生長抑素對大腸癌細胞凋亡的調控可能與Fas/FasL基因的錶達失衡、功能和信號繫統的紊亂有關.
목적 탐토생장억소대대장암세포조망적영향.방법 채용소식RT-PCR방법검측2004년1월지2006년10월환남의학원부속익기산의원수치적79례대장암환자암조직중생장억소mRNA적표체정황,채용면역조직화학법검측대장암조직중생장억소、Fas、FasL、반광천동단백매(caspase)3화8단백적표체정황,TUNEL법검측세포조망지수(AI).채용χ~2검험、q검험、Spearman등급상관검험대결과진행분석.결과 대장암조직중생장억소mRNA여기단백표체정정상관(r=0.98,P<0.05).저분화화중분화대장암조직중생장억소mRNA급기단백적표체명현저우고분화조직(χ~2=10.78,11.24,5.27,5.24,P<0.05);생장억소mRNA급기단백재유두상선암적양성표체솔명현고우점액선암+인계세포암급미분화암(χ~2=6.56,6.99,5.44,7.39,P<0.05);Dukes A、B기적생장억소mRNA급기단백양성표체솔명현고우C、D기(χ~2=5.17,4.06,P<0.05).생장억소고표체조、중표체조적AI명현고우저표체조(q=5.66,4.21,P<0.05);Fas、caspase-8、caspase-3재생장억소고표체조、중표체조적양성표체솔명현고우저표체조(χ~2=5.48,5.62,6.89,4.32,4.19,3.91,P<0.05).결론 생장억소대대장암세포조망적조공가능여Fas/FasL기인적표체실형、공능화신호계통적문란유관.
Objective To investigate the effects of somatostatin on the apoptosis of colorectal cancer cells. Methods The expression of somatostatin mRNA in colorectal cancer tissues from 79 patients who had been admired to Yijishan Hospital from January 2004 to October 2006 was detected by nested RT-PCR. The apoptotic index of colorectal cancer cells was detected by TUNEL, and the protein expressions of somatostatin, Fas, FasL, caspase-3 and caspase-8 in colorectal cancer tissues were detected by immunohistochemistry. All data were analyzed by chi-square test, q test and Spearman rank correlation coefficient. Results There was a positive correlation between the mRNA and protein expression of somatostatin (r = 0.98, P < 0.05). The mRNA and protein expression of somatostatin in poorly and moderately differentiated colorectal cancers were significantly lower than that in well differentiated colorectal cancers (χ~2 = 10.78, 11.24, 5.27, 5.24, P < 0.05). The positive expression rates of mRNA and protein of somatostatin in papillary adenocarcinoma were significantly higher than those in mucinous adenocarcinoma and signet ring cell carcinoma and undifferentiated carcinoma (χ~2= 6.56, 6.99, 5.44, 7.39, P < 0.05). The mRNA and protein expression of somatostatin in colorectal cancer in Dukes A and B were significantly higher than that in Dukes C and D (χ~2 =5.17, 4.06, P <0.05). The apoptotic index in high or moderate somatostatin expression group was significantly higher than that in low somatostain expression group (q = 5.66, 4.21, P < 0.05), and the positive expression rates of Fas, caspase-8 and caspase-3 in high or moderate somatostatin expression group were significantly higher than those in low somatostafin expression group (χ~2= 5.48, 5.62, 6.89, 4.32, 4.19, 3.91, P <0.05). Conclusion Somatostatin plays an important role in the regulation of cell apoptosis in colorectal cancer, and the mechanism may be related to the aberrant expression of Fas/FasL.