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目的:探讨前列腺特异性膜抗原基因复制缺陷型腺病毒(Ad-PSMA)转染的树突状细胞(DC)与细胞因子诱导的杀伤细胞(CIK)共培养后回输体内能否抑制前列腺癌生长。方法:24只免疫缺陷雄性小鼠皮下接种LNcaP细胞构建前列腺癌(PCa)模型。将荷瘤小鼠分成4组,分别回输生理盐水(NS)、CIK、Ad-DC-CIKs以及Ad-PSMA-DC-CIKs,6周后处死小鼠,记录肿瘤重量并行病理学检查和TUNEL凋亡分析。结果:治疗后肿瘤重量在CIK和Ad-DC-CIKs组无显著性差异(P>0.05),其他组间均有显著性差异(P<0.01)。病理学和TUNEL凋亡分析显示NS组PCa腺体结构完整,CIK和Ad-DC-CIKs组移植瘤癌巢部分破坏,而Ad-PSMA-DC-CIKs组癌巢完全破坏,肿瘤细胞片状坏死,凋亡显著。结论:Ad-PSMA负载的DC与CIK共培养回输体内诱导前列腺癌细胞凋亡和坏死,显著抑制肿瘤生长,该研究为PCa尤其是激素难治性PCa提供了一种有效的免疫治疗手段。
OBJECTIVE: To investigate whether reinfection of prostate-specific membrane antigen gene-deficient adenovirus (Ad-PSMA) transfected dendritic cells (DCs) and cytokine-induced killer cells (CIKs) Grow. Methods: Twenty - four immunodeficient male mice were inoculated subcutaneously with LNcaP cells to construct a prostate cancer (PCa) model. The tumor-bearing mice were divided into 4 groups, NS, CIK, Ad-DC-CIKs and Ad-PSMA-DC-CIKs were respectively transfused. After 6 weeks, mice were sacrificed and the tumor weight and pathological examination were performed. TUNEL Apoptosis analysis. Results: There was no significant difference in tumor weight between CIK group and Ad-DC-CIKs group after treatment (P> 0.05). There was significant difference between other groups (P <0.01). Pathological and TUNEL analysis showed that the PCa gland of NS group was intact, while the nest of CIK and Ad-DC-CIKs group was partially destroyed, while the cancer nest of Ad-PSMA-DC-CIKs group was completely destroyed, , Significant apoptosis. CONCLUSION: Ad-PSMA-loaded DC co-cultured with CIK can induce apoptosis and necrosis of prostate cancer cells and significantly inhibit tumor growth. This study provides an effective immunotherapy for PCa, especially hormone-refractory PCa.