Role of c-Myc activating the transcription of PD-L1 in immune escape during benzene-induced malignant transformation of human lymphoblasts.

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.