激肽释放酶-10在甲状腺乳头状癌进展中的作用和调节机制
The Role and Regulatory Mechanism of Kallikrein 10 in Regulating the Progression of Papillary Thyroid Carcinoma
唐海利 1师娇娇 1杨小军 1杨小周 1路建国 1赵华栋1
作者信息
- 1. 710032 空军军医大学第二附属医院
- 折叠
摘要
目的 探究激肽释放酶-10(KLK10)在甲状腺乳头状癌(PTC)进展中的作用和调节机制.方法 实时荧光定量PCR和蛋白免疫印迹法检测PTC患者组织和细胞系中KLK10表达水平.通过CCK-8和Annexin-V/PI凋 亡检测试剂盒分别检测细胞活力和凋亡率.此外,测定各组细胞葡萄糖消耗、乳酸产生和ATP浓度.蛋白免疫印迹检测FAK/SRC/PI3K/AKT轴相关蛋白表达.结果 与正常组相比,PTC组织和细胞中KLK10 mRNA和蛋白水平增加,具有显著性差异(P＜0.01).沉默KLK10细胞活力较对照组减弱,而细胞凋亡较对照组增强.同时,与si-NC组相比,si-KLK10组葡萄糖消耗、乳酸产生和ATP浓度均减少,具有显著性差异(P＜0.01).而KLK10过表达组的结果与沉默KLK10组相反.此外,与对照组相比,KLK10过表达组FAK、SRC、PI3K和AKT的磷酸化水平增加.结论 KLK10通过FAK/SRC/PI3K/AKT轴调节甲状腺乳头状癌患者葡萄糖代谢和恶性进展.
Abstract
Objective To explore the role and underline mechanism of kallikrein-related peptidase 10(KLK10)in pa-pillary thyroid carcinoma(PTC).Methods RT-qPCR and western blot assays were used to detect the expression of KLK10 in PTC tissues and cells.The cell viability and apoptosis rate were detected by CCK-8 and Annexin-V/PI apoptosis detection kits.Besides,glucose uptake,lactate production and ATP concentration were measured in different groups.The FAK/SRC/PI3K/AKT axis related proteins were examined using western blot assay.Results The mRNA and protein expression of KLK10 were in-creased in PTC tissues and cells,compared with normal tissues and cells(P＜0.01).Cell viability in KLK10-silenced group was weaker than control group and cell apoptosis rate was stronger than control group(P＜0.01).Meanwhile,compared with the si-NC group,the glucose uptake,lactate production and ATP concentration were markedly decreased in si-KLK10 group(P＜0.01).The results in the KLK10 overexpression group were opposite to those in the KLK10-silenced group.Moreover,compared with the con-trol group,the phosphorylation levels of FAK,SRC,PI3K and AKT were increased in KLK10 overexpression group.Conclusion KLK10 regulated the glycolysis and progression of papillary thyroid carcinoma patients via FAK/SRC/PI3K/AKT axis.
关键词
激肽释放酶-10/甲状腺乳头状癌/葡萄糖代谢Key words
Kallikrein-related peptidase 10/Papillary thyroid carcinoma/Glucose metabolism引用本文复制引用
基金项目
陕西省自然科学基础研究计划(2022JM-604)
出版年
2024
NETL
NSTL
万方数据