SIRT7 通过调节 KIF23 的去琥珀酰化来促进间变性甲状腺癌细胞的增殖和迁移。
SIRT7 promotes the proliferation and migration of anaplastic thyroid cancer cells by regulating the desuccinylation of KIF23.
机构信息
Department of Vascular and Thyroid Surgery, The Affiliated Hospital of Guangdong Medical University, No. 57, South Renmindadao, Xiashan District, Zhanjiang, Guangdong, 524001, China.
Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
出版信息
BMC Cancer. 2024 Feb 15;24(1):210. doi: 10.1186/s12885-024-11965-9.
OBJECTIVE
This study was designed to investigate the regulatory effects of kinesin family member (KIF) 23 on anaplastic thyroid cancer (ATC) cell viability and migration and the underlying mechanism.
METHODS
Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to analyze the levels of KIF23 in ATC cells. Besides, the effects of KIF23 and sirtuin (SIRT) 7 on the viability and migration of ATC cells were detected using cell counting kit-8, transwell and wound healing assays. The interaction between SIRT7 and KIF23 was evaluated by co-immunoprecipitation (Co-IP) assay. The succinylation (succ) of KIF23 was analyzed by western blot.
RESULTS
The KIF23 expression was upregulated in ATC cells. Silencing of KIF23 suppressed the viability and migration of 8505C and BCPAP cells. The KIF23-succ level was decreased in ATC cells. SIRT7 interacted with KIF23 to inhibit the succinylation of KIF23 at K537 site in human embryonic kidney (HEK)-293T cells. Overexpression of SIRT7 enhanced the protein stability of KIF23 in HEK-293T cells. Besides, overexpression of KIF23 promoted the viability and migration of 8505C and BCPAP cells, which was partly blocked by silenced SIRT7.
CONCLUSIONS
SIRT7 promoted the proliferation and migration of ATC cells by regulating the desuccinylation of KIF23.
目的
本研究旨在探讨驱动蛋白家族成员（KIF）23 对间变性甲状腺癌（ATC）细胞活力和迁移的调节作用及其机制。
方法
采用反转录-定量聚合酶链反应（RT-qPCR）分析 ATC 细胞中 KIF23 的水平。此外，通过细胞计数试剂盒-8（CCK-8）、Transwell 和划痕愈合实验检测 KIF23 和 SIRT7 对 ATC 细胞活力和迁移的影响。通过免疫共沉淀（Co-IP）实验评估 SIRT7 与 KIF23 的相互作用。通过 Western blot 分析 KIF23 的琥珀酰化（succ）水平。
结果
KIF23 在 ATC 细胞中表达上调。沉默 KIF23 抑制 8505C 和 BCPAP 细胞的活力和迁移。ATC 细胞中 KIF23-succ 水平降低。SIRT7 与 KIF23 相互作用，抑制人胚肾（HEK）-293T 细胞中 KIF23 在 K537 位的琥珀酰化。SIRT7 的过表达增强了 HEK-293T 细胞中 KIF23 的蛋白稳定性。此外，过表达 KIF23 促进了 8505C 和 BCPAP 细胞的活力和迁移，而沉默 SIRT7 部分阻断了这一作用。
结论
SIRT7 通过调节 KIF23 的去琥珀酰化来促进 ATC 细胞的增殖和迁移。
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