SYVN1 通过使 HMGB1 不稳定来调节甲状腺乳头状癌的进展。
SYVN1 modulates papillary thyroid carcinoma progression by destabilizing HMGB1.
作者信息
Duan Fei, Kong Fanli, Jiang Taifeng, Liu Hongbing
机构信息
Department of Otolaryngology Head and Neck Surgery, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330006, China.
Department of Otolaryngology Head and Neck Surgery, Jiujiang First People's Hospital, Jiujiang, 332600, China.
出版信息
Cell Div. 2024 Apr 28;19(1):15. doi: 10.1186/s13008-024-00121-1.
E3 ubiquitin ligase synoviolin (SYVN1) has been reported to participate in many human cancers. This study aimed to investigate SYVN1's roles and molecular pathways in papillary thyroid cancer (PTC). The functions of SYVN1 in PTC were further analyzed using gain- and loss-of-function methods and numerous investigations in cellular function and molecular biology. The findings demonstrated that the overexpression of SYVN1 markedly suppressed the proliferation, migration, and invasion of PTC cell lines (NPA87 and TPC-1). We found that SYVN1 interacted with HMGB1 and promoted its ubiquitination and degradation. In addition, SYVN1 effectively impairs cell proliferation, migration, invasion, and the formation of tumor xenografts in mice models. However, this effect may be partly reversed by overexpressing HMGB1. Thus, SYVN1 may inhibit the proliferation, migration, and invasion of PTC cells by disrupting HMGB1. Consequently, SYVN1 might be considered a promising therapeutic target for PTC.
据报道，E3泛素连接酶滑膜素（SYVN1）参与多种人类癌症。本研究旨在探讨SYVN1在甲状腺乳头状癌（PTC）中的作用及分子途径。采用功能获得和功能缺失方法以及细胞功能和分子生物学方面的大量研究，进一步分析了SYVN1在PTC中的功能。研究结果表明，SYVN1的过表达显著抑制了PTC细胞系（NPA87和TPC-1）的增殖、迁移和侵袭。我们发现SYVN1与高迁移率族蛋白B1（HMGB1）相互作用，并促进其泛素化和降解。此外，SYVN1有效地损害了小鼠模型中的细胞增殖、迁移、侵袭以及肿瘤异种移植的形成。然而，过表达HMGB1可能会部分逆转这种作用。因此，SYVN1可能通过破坏HMGB1来抑制PTC细胞的增殖、迁移和侵袭。因此，SYVN1可能被认为是PTC的一个有前景的治疗靶点。
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