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微小RNA-7a是死亡结构域相关蛋白（FADD）调控的粘着斑激酶（FAK）表达中的重要介质。

MiR-7a is an important mediator in Fas-associated protein with death domain (FADD)-regulated expression of focal adhesion kinase (FAK).

作者信息

Liu Yingting, Cui Hongen, Huang Xianjie, Zhu Bo, Guan Shengwen, Cheng Wei, Lai Yueyang, Zhang Xiaoxin, Hua Zi-Chun

机构信息

The State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences and School of Stomatology, Affiliated Stomatological Hospital, Nanjing University, Nanjing, 210032, China.

Changzhou High-Tech Research Institute of Nanjing University and Jiangsu TargetPharma Laboratories Inc., Changzhou, 213164, China.

出版信息

Oncotarget. 2016 Aug 9;7(32):51393-51407. doi: 10.18632/oncotarget.9838.

DOI:10.18632/oncotarget.9838
PMID:27286445
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5239483/
Abstract

Fas-associated protein with death domain (FADD), a classical adaptor protein mediating apoptotic stimuli-induced cell death, has been reported to engage in several non-apoptotic processes such as T cell and cardiac development and tumorigenesis. Recently, there are several reports about the FADD's involvement in cell migration, however the underlying mechanism remains elusive. Here, we present a new finding that FADD could regulate the expression of FAK, a non-receptor protein tyrosine kinase overexpressed in many cancers, and played an important role in cell migration in murine MEF and melanoma cells with different metastatic potential, B16F10 and B16F1. Moreover, miR-7a, a tumor suppressor which prohibits cell migration and invasion, was up-regulated in FADD-deficient cells. And FAK was verified to be the direct target gene of miR-7a in B16F10 cells. Furthermore, we demonstrate that miR-7a was a necessary mediator in FADD-regulated FAK expression. In contrast to its classical apoptotic role, FADD interference could reduce the rate of cell migration, which could be rescued by inhibiting miR-7a expression. Taken together, our data provide a novel explanation regarding how FADD regulates cell migration in murine melanoma cells.

摘要

死亡结构域相关蛋白（FADD）是一种介导凋亡刺激诱导细胞死亡的经典衔接蛋白，据报道它参与了多种非凋亡过程，如T细胞和心脏发育以及肿瘤发生。最近，有几篇关于FADD参与细胞迁移的报道，但其潜在机制仍不清楚。在此，我们提出一项新发现，即FADD可调节粘着斑激酶（FAK）的表达，FAK是一种在许多癌症中过表达的非受体蛋白酪氨酸激酶，并且在具有不同转移潜能的小鼠成纤维细胞（MEF）和黑色素瘤细胞B16F10及B16F1的细胞迁移中发挥重要作用。此外，miR - 7a是一种抑制细胞迁移和侵袭的肿瘤抑制因子，在FADD缺陷细胞中上调。并且在B16F10细胞中，FAK被证实是miR - 7a的直接靶基因。此外，我们证明miR - 7a是FADD调节FAK表达的必要介质。与其经典的凋亡作用相反，FADD干扰可降低细胞迁移速率，而抑制miR - 7a表达可挽救这一现象。综上所述，我们的数据为FADD如何调节小鼠黑色素瘤细胞中的细胞迁移提供了一种新的解释。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/030d/5239483/017d1649f71b/oncotarget-07-51393-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/030d/5239483/dbde87b9f462/oncotarget-07-51393-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/030d/5239483/e2d98886eebe/oncotarget-07-51393-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/030d/5239483/3ecc87589367/oncotarget-07-51393-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/030d/5239483/ce77f6063e67/oncotarget-07-51393-g003.jpg
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