Chen Xianjie, Xu Zhenyuan, Lu Meng, Ding Wenjun, Zhong Jun, Deng Suihui, Li Siyan, Miao Jifei, Liu Xiaoyi, Wen Quan, Ye Sen, Li Chun, Li Hui
School of Basic Medical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510006, PR China; Department of Human Anatomy, School of Basic Medical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510006, PR China.
School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen, 518055, PR China.
Biochem Biophys Res Commun. 2023 May 14;656:86-96. doi: 10.1016/j.bbrc.2023.03.005. Epub 2023 Mar 5.
The abnormal immune response mediated by malignant melanoma is related to PD1. Paeonol has pharmacological antitumor activity. Previous studies have indicated that paeonol induces tumor cell apoptosis, but its underlying mechanism in tumor immunity remains unknown. In this study, malignant melanoma was established in normal and thymectomized mice to determine the important role of the thymus in the antitumor effects of paeonol. Paeonol-treated thymocytes were cocultured with melanoma cell spheres to further evaluate the regulatory role of thymocytes in tumor immune dysfunction. Studies have shown that PD1 may be targeted by miR-139-5p. Our results revealed that tumor-induced thymic atrophy was significantly accompanied by high PD1 expression and low miR-139-5p expression. Interestingly, paeonol significantly reversed thymic atrophy and largely protected thymocytes against low PD1 expression and high miR-139-5p expression. Dual-luciferase assays indicated that miR-139-5p interacted with the 3' untranslated region (3'-UTR) of PD1. These results showed that paeonol alleviates PD1-mediated antitumor immunity by reducing miR-139-5p expression and demonstrated a novel mechanism for melanoma immunotherapy.
由恶性黑色素瘤介导的异常免疫反应与程序性死亡受体1(PD1)有关。丹皮酚具有药理抗肿瘤活性。先前的研究表明,丹皮酚可诱导肿瘤细胞凋亡,但其在肿瘤免疫中的潜在机制仍不清楚。在本研究中,在正常和胸腺切除的小鼠中建立恶性黑色素瘤模型,以确定胸腺在丹皮酚抗肿瘤作用中的重要作用。将经丹皮酚处理的胸腺细胞与黑色素瘤细胞球共培养,以进一步评估胸腺细胞在肿瘤免疫功能障碍中的调节作用。研究表明,miR-139-5p可能靶向PD1。我们的结果显示,肿瘤诱导的胸腺萎缩显著伴随着高PD1表达和低miR-139-5p表达。有趣的是,丹皮酚显著逆转了胸腺萎缩,并在很大程度上保护胸腺细胞免受低PD1表达和高miR-139-5p表达的影响。双荧光素酶报告基因检测表明,miR-139-5p与PD1的3'非翻译区(3'-UTR)相互作用。这些结果表明,丹皮酚通过降低miR-139-5p表达减轻PD1介导的抗肿瘤免疫,并为黑色素瘤免疫治疗证明了一种新机制。