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Plac1 promotes nasopharyngeal carcinoma cells proliferation, migration and invasion via Furin/NICD/PTEN pathway
Tissue & Cell ( IF 2.7 ) Pub Date : 2021-01-05 , DOI: 10.1016/j.tice.2020.101480
Chuanbao Lin 1 , Pengfei Qian 2 , Yan Zhang 3 , Zhihui Liu 1 , Kun Dai 4 , Dawei Sun 1
Affiliation  

Placenta-specific protein 1 (Plac1) has critical functions in multiple human malignancies, but its role in nasopharyngeal carcinoma (NPC) was unclear. Clinical samples of NPC and adjacent normal tissue were collected. Plac1 expressions in both tissues and cells were measured. After cell transfection, NPC cell viability, proliferation, migration and invasion were detected using cell counting kit-8 (CCK-8) assay, colony formation assay, scratch assay and Transwell assay. Relative expressions of Plac1 and proteins related to migration and invasion (E-Cadherin, N-cadherin, Matrix metalloproteinase2 (MMP2), and MMP9), Furin/Notch1 intracellular domain (NICD)/phosphate and tension homology (PTEN) pathway (NICD, PTEN, phosphorylated-Akt (p-Akt), Akt) were quantified by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot as needed. The interaction between Plac1 and Furin, a member of Furin/NICD/PTEN Pathway, was analyzed using co-Immunoprecipitation (co-IP) assay. Plac1 expression was upregulated in both NPC tissue and cells. Overexpressed Plac1 promoted Plac1 and Furin expressions and increased cell viability, proliferation, migration and invasion of NPC cells, while silencing Plac1 showed the opposite effects. Plac1 interacted with Furin, overexpression of Furin reversed the inhibitory effects of silencing Plac1 on NPC cell proliferation, migration, and invasion, and also reversed the effects of silencing Plac1 on Furin/NICD/PTEN pathway-, cell migration-, and invasion-related protein expressions. Plac1 promoted NPC cell proliferation, migration and invasion via Furin/NICD/PTEN Pathway. The findings of this study provide a possible therapeutic method for NPC treatment.



中文翻译:

Plac1通过Furin/NICD/PTEN通路促进鼻咽癌细胞增殖、迁移和侵袭

胎盘特异性蛋白 1 (Plac1) 在多种人类恶性肿瘤中具有关键功能,但其在鼻咽癌 (NPC) 中的作用尚不清楚。收集鼻咽癌和邻近正常组织的临床样本。测量了组织和细胞中的 Plac1 表达。细胞转染后,使用细胞计数试剂盒-8(CCK-8)测定、集落形成测定、划痕测定和Transwell测定检测NPC细胞的活力、增殖、迁移和侵袭。Plac1 和与迁移和侵袭相关的蛋白质(E-Cadherin、N-cadherin、Matrix metalloproteinase2 (MMP2) 和 MMP9)、Furin/Notch1 细胞内结构域 (NICD)/磷酸盐和张力同源性 (PTEN) 通路(NICD, PTEN、磷酸化-Akt (p-Akt)、Akt) 根据需要通过定量实时聚合酶链反应 (qRT-PCR) 和蛋白质印迹进行定量。使用共免疫沉淀 (co-IP) 测定分析 Plac1 和弗林蛋白酶 (Furin/NICD/PTEN 通路的成员) 之间的相互作用。Plac1 表达在 NPC 组织和细胞中均上调。过表达的 Plac1 促进了 Plac1 和 Furin 的表达,并增加了 NPC 细胞的细胞活力、增殖、迁移和侵袭,而沉默 Plac1 则显示出相反的效果。Plac1 与 Furin 相互作用,Furin 的过表达逆转了沉默 Plac1 对 NPC 细胞增殖、迁移和侵袭的抑制作用,也逆转了沉默 Plac1 对 Furin/NICD/PTEN 通路、细胞迁移和侵袭相关的影响蛋白质表达。Plac1 通过 Furin/NICD/PTEN 通路促进 NPC 细胞增殖、迁移和侵袭。本研究的结果为鼻咽癌的治疗提供了一种可能的治疗方法。

更新日期:2021-01-05
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