Original experimental data.part08.

Benzene is a widely used industrial raw material. Benzene and its metabolite hydroquinone are believed to be related to the occurrence of benzene-related leukemia. Epidemiological studies have revealed the link between benzene exposure and blood system tumors, but the mechanism of benzene exposure and blood system tumor immune escape has not been fully confirmed. Experiments are divided into in vitro experiments and in vivo experiments. In the in vivo experimental part, we constructed an animal model of chronic benzene exposure and a C57BL/6 tumor-like animal model. Through qRT-PCR, Western blot and Tumor formation experiment in C57BL/6 mice, we verified that chronic benzene exposure caused malignant lesions in mice. In in vitro experiments, we built an in vitro malignant transformation model. Through molecular biology experiments 9/3/20259/3/20259/3/20259/3/2025such as CCK-8, soft agar cloning, and Transwell experiments were conducted to assess the malignant transformation potential of HQ19 and PBS19, cell vitality, malignant transformation potential and malignant migration ability were detected respectively. In order to study whether the benzene metabolite HQ activates c-Myc transcription activity, we used experiments such as double fluoresin enzyme reporting genes to confirm that c-Myc directly binds to PD-L1 promoter to drive its transcription. This study confirmed that in the process of HQ induced malignant transformation of human lymphocytes TK6, c-Myc regulates the molecular mechanism of PD-L1-mediated immune escape through transcription.苯是一种广泛应用的工业原料。苯及其代谢物氢醌（hydroquinone）被认为与苯相关性白血病的发生密切相关。流行病学研究已揭示苯暴露与血液系统肿瘤之间的关联，但苯暴露诱发血液系统肿瘤免疫逃逸的具体机制尚未完全阐明。 本研究分为体外实验与体内实验两部分。体内实验部分，我们构建了慢性苯暴露动物模型及C57BL/6肿瘤荷瘤动物模型；通过qRT-PCR、蛋白质免疫印迹（Western blot）及C57BL/6小鼠成瘤实验，验证了慢性苯暴露可诱导小鼠发生恶性病变。体外实验中，我们建立了体外恶性转化模型，采用CCK-8、软琼脂克隆、Transwell等分子生物学实验手段，分别检测HQ19与PBS19细胞的细胞活力、恶性转化潜能及恶性迁移能力。为探究苯代谢物氢醌是否可激活c-Myc转录活性，我们通过双荧光素酶报告基因等实验证实，c-Myc可直接结合PD-L1启动子并驱动其转录。本研究明确了在苯代谢物氢醌诱导人淋巴细胞TK6发生恶性转化的过程中，c-Myc通过转录调控PD-L1介导免疫逃逸的分子机制。