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中文摘要：
弥漫大B细胞淋巴瘤是最常见的恶性淋巴瘤亚型。PRDM1基因在B细胞分化过程中发挥重要作用，包含PRDM1α和β两种亚型。为进一步阐明PRDM1β对淋巴瘤细胞生物学行为和治疗药物反应的影响，本课题设计了能够有效下调PRDM1β表达的siRNA。PRDM1β表达下调后，淋巴瘤细胞对化疗药物阿霉素的敏感性增加，凋亡细胞比例和G2/M期细胞比例明显升高。体内试验中裸鼠移植瘤经阿霉素治疗后，接种干扰序列的肿瘤体积较接种对照序列者明显缩小。机制研究显示，PRDM1β通过抑制P53表达，影响肿瘤细胞凋亡、周期，使肿瘤细胞对药物敏感性增加，为淋巴瘤靶向治疗提供了新的靶点。同时，我们也对PRDM1β的表观遗传学调控进行了研究。通过重亚硫酸盐测序PCR检测细胞株以及MassARRAY技术筛选患者PRDM1β启动子区的甲基化，结果显示，PRDM1β启动子区的CpG岛具有转录活性，且可受甲基化调控。与反应性增生相比，淋巴瘤中PRDM1β启动子区的甲基化缺失较多，率先报道抑癌基因功能异常的异构体去甲基化是导致淋巴瘤疾病进展的可能机制。
结论摘要：
英文主题词Lymphoma；PRDM1 gene；Chemosensitivity；Epigenetics
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