1Department of General Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, China
2Department of General Surgery, Zhongshan Hospital (Xiamen), Fudan University, Xiamen 361015, China
3Xiamen Clinical Research Center for Cancer Therapy, Xiamen 361015, China
Abstract
This study addresses a critical knowledge gap in understanding the tumor microenvironment of thyroid cancer by elucidating the mechanism by which tumor cell-derived CD133-positive exosomes promote lymph node metastasis. We employed molecular docking, western blot, and other molecular characterizations to investigate the crucial interaction between CD133 and VEGFR3 and its impact on metastasis. Additionally, experiments assessed the influence of CD133-positive exosomes on lymphatic endothelial cell proliferation and migration.
Our findings demonstrate a significant direct interaction between CD133 and VEGFR3, as suggested by molecular docking. Furthermore, inhibition of CD133 expression resulted in a notable reduction in lymph node metastasis. We also observed that CD133-positive exosomes derived from thyroid cancer cells actively contribute to the migration and proliferation of lymphatic endothelial cells.
These results unveil a novel pathway for lymph node metastasis in thyroid cancer. The identification of CD133 and its interaction with VEGFR3 as key players in this process holds significant promise for the development of targeted therapeutic strategies. By focusing on these targets, researchers can potentially improve the prognosis of patients with thyroid cancer.
Keywords: Thyroid cancer cells, Exomes, Lymph node metastasis, CD133, VEGFR3
