无缺口同系物1调控PI3K/AKT通路对鼻咽癌细胞迁移与侵袭能力的影响OACSTPCD
Effects of Notchless homolog 1 through regulating PI3K/AKT pathway on migration and invasion of nasopharyngeal carcinoma cells
目的:探究无缺口同系物1(NLE1)通过PI3K/AKT通路对鼻咽癌细胞迁移和侵袭能力的影响.方法:将鼻咽癌细胞HK-1细胞与C666-1细胞分别转染sh-NC和sh-NLE1,分为NC(空白对照)组和sh-NLE1组;免疫印迹检测HK-1细胞和C666-1细胞中NLE1、磷脂酰肌醇3激酶(PI3K)、蛋白激酶B(AKT)、基质金属蛋白酶2(MMP2)、基质金属蛋白酶9(MMP9)的蛋白表达水平.用Transwell法与细胞划痕实验检测HK-1细胞和C666-1细胞的迁移与侵袭能力.裸鼠荷瘤实验检测肿瘤的生长情况.结果:与NC组比较,sh-NLE1组HK-1细胞和C666-1细胞中NLE1、PI3K、AKT、MMP2和MMP9蛋白表达水平显著降低.与NC组比较,sh-NLE1组HK-1细胞和C666-1细胞的迁移与侵袭能力显著降低.与NC组比较,sh-NLE1组HK-1细胞和C666-1细胞的成瘤体积显著降低.结论:抑制鼻咽癌细胞NLE1的表达,可介导PI3K/AKT通路影响鼻咽癌细胞的迁移和侵袭能力,进而抑制鼻咽癌的生长与发展.
Objective:To explore the effects of Notchless homolog 1(NLE1)on the migration and invasion ability of nasopharyngeal carcinoma(NPC)cells through PI3K/AKT pathway.Methods:HK-1 cells and C666-1 cells were transfected with sh-NC and sh-NLE1,respectively,and divided into NC(negative control)group and sh-NLE1 group.Western blotting was used to detect the protein expression levels of NLE1,PI3K,AKT,MMP2,and MMP9 in HK-1 and C666-1 cells.The migration and invasion ability of HK-1 and C666-1 cells were detected by Transwell assay and cell scratch assay.Nude mice with xenograft tumors were used to assess the growth status of tumors.Results:Compared with the NC group,the protein expression levels of NLE1,PI3K,AKT,MMP2 and MMP9 in HK-1 and C666-1 cells in the sh-NLE1 group were significantly decreased.The migration and invasion ability of HK-1 and C666-1 cells in the sh-NLE1 group were significantly weakened compared with the NC group.Compared with the NC group,the tumor volumes of HK-1 and C666-1 cells in the sh-NLE1 group were significantly reduced.Conclusion:The inhibition of NLE1 expression in NPC cells can mediate the PI3K/AKT pathway and affect the migration and invasion ability of NPC cells,thus inhibiting the growth and development of NPC.
徐凯;孙晋发;尚兴国
秦皇岛市第四医院头颈外科,秦皇岛 066000
临床医学
无缺口同系物1鼻咽癌磷脂酰肌醇3激酶蛋白激酶B
Notchless homolog 1nasopharyngeal carcinomaPI3KAKT
《解剖学杂志》 2024 (004)
328-332 / 5
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