中文摘要：

目的通过包含SSTR2基因的重组腺病毒（AdCAG—SSTR2）转染人胰腺癌细胞，观察对胰腺癌细胞肿瘤特性的影响。方法分别应用空载体、AdCAG—SSTR2转染SSTR2阴性的人胰腺癌细胞株BxPC-3。逆转录-聚合酶链反应（RT—PCR）和Western blot法分析检测SSTR2在细胞中的表达。非转染细胞、转染空载体细胞和转染AdCAG—SSTR2细胞直接计数测定细胞生长速度。采用膜联蛋白V／碘化丙锭（Annexin V／PI）标记法检测细胞凋亡。RT—PCR检测PCNA、bax和bel-xl的表达。结果AdCAG—SSTR2转染胰腺癌细胞后可以检测到SSTR2mRNA和蛋白的稳定表达，转染AdCAG．SSTR2后细胞生长受到抑制，与对照组差异有统计学意义（P〈0．01）；细胞凋亡率较对照组明显升高（P〈0．01）；PCNA的表达无明显变化，是对照组的1．04倍；bax的表达明显升高，是对照组的3．18倍；bel-xl的表达明显降低，是对照组的0．34倍。结论SSTR2通过诱导胰腺癌细胞凋亡发挥抗肿瘤增殖的作用，其机制与上调bax的表达，下调bcl-xl的表达有关。

英文摘要：

Objective By correcting the somatostatin receptor subtype 2 （SSTR2） defect in human pancreatic cancer BxPC-3 cells by stable transfection with adcnoviral vector containing the SSTR2,to investigate its effect on tumorigenicity of human pancreatic cancer, and elucidate the underlying mechanisms. Methods AdCAG-SSTR2 and empty vector were transfected somatostatin receptor-negative human pancreatic cancer cells （ BxPC-3 ） respectively. The expression of SSTR2 was detected by RT-PCR and Western blot. Negative contral, vector control, and SSR2 transfected cells were cultured, and the rate of cell growth was determined by direct cell counting using a hemacytometer. The apoptosis was assessed by flow cytometric Annexin V/PI labelling assay. The expression of PCNA, bax and bd-xl was detected by real time PCR. Results The stable expression of SSTR2 was detected in the cells transfected with AdCAGSSR2. The pancreatic cancer cell growth was significantly decreased in experimental group as compared with control groups （ P 〈 0.01 ）. The apoptosis rate was significantly increased in cells re-expressing SSTR2 （9.45%） as compared with control group （ P 〈 0.01 ）. The expression levels of bax was significantly increased to 3.18 fold, and that of bcl-xl markedly reduced to 0.34 fold in comparison to control group. Conclusion SSTR2 exerts its antitumor effect against proliferation through inducing apoptosis of pancreatic cancer cells,which is related to the up-regulation of the bax expression and down-regulation of the bcl-xl expression.