Division of Oral and Maxillofacial Surgery, Faculty of Dentistry, The University of Hong Kong, Hong Kong.
The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST KLOS) & Key Laboratory of Oral Biomedicine Ministry of Education (KLOBME), School & Hospital of Stomatology, Wuhan University, Wuhan, China; Department of Periodontology, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Biochim Biophys Acta Mol Basis Dis. 2023 Jun;1869(5):166695. doi: 10.1016/j.bbadis.2023.166695. Epub 2023 Mar 22.
Invasion and migration are significant challenges for treatment of oral squamous cell carcinomas (OSCCs). Tumor-associated macrophages (TAMs) interact with cancer cells and are involved in tumor progression. Our recent study demonstrated that melatonin inhibits OSCC invasion and migration; however, the mechanism by which melatonin influences crosstalk between TAMs and OSCCs is poorly understood. In this study, a co-culture system was established to explore the interactions between human monocytic cells (THP-1 cells) and human tongue squamous cell carcinoma cells (SCC-15 cells). The results were verified using monocyte-derived macrophages (MDMs) isolated and differentiated from primary peripheral blood mononuclear cells. In vivo, assays were performed to confirm the anticancer effects of melatonin. SCC-15 cells co-cultured with THP-1 cells or MDMs exhibited increased migration and invasion, which was reversed by melatonin. Co-culture also increased the expression of macrophage migration inhibitory factor (MIF), CD40, CD163 and IL-1β, and these changes were also reversed by melatonin. Moreover, IL-1β secretion in THP-1 cells was MIF- and NLR family pyrin domain-containing 3 (NLRP3)-dependent, and treated with IL-1β enhanced the invasion and migration of SCC-15 cells. Furthermore, melatonin treatment significantly decreased tumor volumes and weights, and tumors from mice treated with melatonin had lower levels of MIF, NLRP3, and IL-1β than tumor from control mice. These results demonstrate that macrophages facilitate the progression of OSCCs by promoting the MIF/NLRP3/IL-1β signaling axis, which can be interrupted by melatonin. Therefore, melatonin could act as an alternative anticancer agent for OSCCs by targeting this signaling axis.
侵袭和迁移是口腔鳞状细胞癌 (OSCC) 治疗的重大挑战。肿瘤相关巨噬细胞 (TAMs) 与癌细胞相互作用,并参与肿瘤的进展。我们最近的研究表明,褪黑素抑制 OSCC 的侵袭和迁移;然而,褪黑素影响 TAMs 和 OSCC 之间串扰的机制尚不清楚。在这项研究中,建立了共培养系统来探索人单核细胞 (THP-1 细胞) 和人舌鳞状细胞癌细胞 (SCC-15 细胞) 之间的相互作用。使用从原代外周血单核细胞分离和分化的单核细胞来源的巨噬细胞 (MDMs) 验证了结果。在体内,进行了实验来确认褪黑素的抗癌作用。与 THP-1 细胞或 MDMs 共培养的 SCC-15 细胞表现出迁移和侵袭增加,这一现象被褪黑素逆转。共培养还增加了巨噬细胞移动抑制因子 (MIF)、CD40、CD163 和 IL-1β 的表达,这些变化也被褪黑素逆转。此外,THP-1 细胞中的 IL-1β 分泌依赖于 MIF 和 NLR 家族富含 pyrin 结构域蛋白 3 (NLRP3),用 IL-1β 处理增强了 SCC-15 细胞的侵袭和迁移。此外,褪黑素治疗显著降低了肿瘤体积和重量,并且褪黑素治疗的小鼠的肿瘤中 MIF、NLRP3 和 IL-1β 的水平低于对照组小鼠的肿瘤。这些结果表明,巨噬细胞通过促进 MIF/NLRP3/IL-1β 信号通路促进 OSCC 的进展,而褪黑素可以阻断该信号通路。因此,褪黑素可以通过靶向该信号通路作为 OSCC 的替代抗癌药物。