Myosin-10 promotes angiogenesis and malignant phenotypes in thyroid cancer through functional association with the FGF/FGFR1 signaling axis
Year: 2026
Type: article
Abstract: Thyroid cancer (TC) is the most prevalent endocrine malignancy globally, with angiogenesis and metastasis-driven aggressive progression posing a major clinical challenge. Myosin-10 (MYH10), involved in tumor cell motility and cytoskeletal rearrangement, has unclear functional roles and mechanisms in TC angiogenesis and metastasis. This study aimed to investigate MYH10’s function and its mediation by the FGF/FGFR1 signaling axis. A stable MYH10 knockdown model was established in human papillary thyroid carcinoma K1 cells; cell proliferation, migration, and invasion were assessed via CCK-8, scratch wound healing, and Transwell assays, with FGF3/FGFR1 detected by Western blot. Human umbilical vein endothelial cells (HUVECs) were treated with conditioned medium from MYH10-knocked-down K1 cells or directly transfected with MYH10 shRNA, followed by VEGFA/CD31 immunofluorescence and tube formation assays. Nude mouse subcutaneous tumor models were established, with HE staining, IHC (VEGFA/CD31/Ki67), WB, single-cell RNA sequencing (scRNA-seq), and CoIP-MS performed. MYH10 knockdown inhibited K1 cell functions, downregulated FGF3/FGFR1, reduced HUVECs’ VEGFA/CD31 expression and tube formation, and suppressed tumor growth/angiogenesis in vivo. CoIP-MS identified FGFR1 as a MYH10-interacting protein (1 unique peptide, 0.68% sequence coverage, adjusted P = 0.003; no MYH10-FGF3 binding). scRNA-seq showed altered tumor microenvironment heterogeneity (reduced pro-angiogenic ECs/TAMs, increased quiescent fibroblasts, downregulated angiogenesis genes).
Source: Scientific Reports
Authors: Wenkai Duan, Wenli Gao, Weihua Zhan, Meiyu Gu, Lingyao Peng
Language: English
Subfield: Endocrinology, Diabetes and Metabolism
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,690
OpenAlex ID: W7204222645