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目的:研究腺病毒介导的IL-24基因表达对前列腺癌细胞体内外的抑癌效应及分子机制。方法:将扩增的Ad-IL-24感染PC-3细胞,用RT-PCR和Western blot法检测IL-24基因在PC-3细胞中的表达;MTT法检测IL-24基因表达对PC-3细胞的生长影响;流式细胞术(FCM)检测细胞凋亡变化;RT-PCR法检测IL-24基因的表达对PC-3细胞中的Bcl-2、Bax、p53和Caspase3凋亡相关基因表达的影响。用Ad-IL-24在裸鼠PC-3移植瘤的瘤体内注射治疗,通过免疫组化法检测Bcl-2、Bax、Caspase-3、CD34等与细胞凋亡和血管形成相关因子的表达。结果:IL-24基因在PC-3细胞中成功表达,对PC-3细胞增殖有明显抑制作用,可上凋p53、Bax、Caspase-3基因和下凋Bcl-2基因表达,进而诱导细胞凋亡。Ad-IL-24能显著抑制裸鼠前列腺癌移植瘤生长,瘤重的抑制率可达54%;免疫组化结果显示Ad-IL-24不仅能明显上调Bax和Caspase-3基因和下调Bcl-2基因表达,而且能引起与血管形成标记基因CD34表达水平下降。结论:腺病毒介导的IL-24基因表达在体内外可明显抑制PC-3细胞的生长,诱导其凋亡。其机制可能与上凋P53、Bax、Caspase-3基因和下凋Bcl-2和CD34基因表达水平有关。
Objective: To study the anti-cancer effect and molecular mechanism of adenovirus-mediated IL-24 gene expression on prostate cancer cells in vitro and in vivo. Methods: PC-3 cells were infected with Ad-IL-24. The expression of IL-24 gene in PC-3 cells was detected by RT-PCR and Western blot. The expression of IL- 3 cells were detected by flow cytometry. Apoptotic changes were detected by flow cytometry (FCM). Apoptosis-related genes of Bcl-2, Bax, p53 and Caspase3 in PC-3 cells were detected by RT- The impact of expression. The expression of Bcl-2, Bax, Caspase-3, CD34 and other factors related to apoptosis and angiogenesis was detected by immunohistochemistry in nude mouse PC-3 xenografts with Ad-IL-24. Results: The successful expression of IL-24 gene in PC-3 cells could significantly inhibit the proliferation of PC-3 cells and up-regulate the expressions of p53, Bax, Caspase-3 and Bcl-2 genes, Death. Ad-IL-24 could significantly inhibit the growth of transplanted prostate cancer in nude mice, and the inhibition rate of tumor weight was up to 54%. Immunohistochemistry showed that Ad-IL-24 could not only significantly up-regulate Bax and Caspase-3 genes but also down- 2 gene expression, and can cause the expression of angiogenesis marker gene CD34 decreased. Conclusion: Adenovirus-mediated IL-24 gene expression can significantly inhibit the growth of PC-3 cells in vitro and in vivo and induce apoptosis. The mechanism may be related to up-regulation of P53, Bax, Caspase-3 genes and down-regulation of Bcl-2 and CD34 gene expression.