当前位置: X-MOL 学术Cell Adhes. Migr. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Fluid shear stress induces cell migration and invasion via activating autophagy in HepG2 cells.
Cell Adhesion & Migration ( IF 3.2 ) Pub Date : 2019-01-31 , DOI: 10.1080/19336918.2019.1568141
Zhiping Yan 1 , Guanyue Su 1 , Wenbo Gao 1 , Jia He 1 , Yang Shen 1 , Ye Zeng 1 , Xiaoheng Liu 1
Affiliation  

Fluid shear stress (FSS) regulates the metastasis of hepatocellular carcinoma (HCC). In the present study, we aimed to study the role of autophagy in HCC cells under FSS. The results showed that FSS upregulated the protein markers of autophagy, induced LC3B aggregation and formation of autophagosomes. Inhibition of integrin by Cliengitide (Cli) or inhibition of the microfilaments formation both inhibited the activation of autophagy in HepG2 under FSS. In addition, Cli inhibited the microfilaments formation and expressions of Rac1 and RhoA in HepG2 cells under FSS. Finally, inhibition of autophagy suppressed the cell migration and invasion in HepG2 under FSS. In conclusion, FSS induced autophagy to promote migration and invasion of HepG2 cells via integrin/cytoskeleton pathways.

中文翻译:

流体剪切应力通过激活HepG2细胞中的自噬来诱导细胞迁移和侵袭。

流体剪切应力(FSS)调节肝细胞癌(HCC)的转移。在本研究中,我们旨在研究自噬在FSS下HCC细胞中的作用。结果表明,FSS上调了自噬的蛋白质标记,诱导了LC3B的聚集和自噬体的形成。Cliengitide(Cli)对整联蛋白的抑制或微丝形成的抑制均抑制了FSS下HepG2中自噬的激活。此外,Cli抑制了FSS下HepG2细胞中微丝的形成以及Rac1和RhoA的表达。最后,自噬的抑制抑制了FSS下HepG2中的细胞迁移和侵袭。总之,FSS诱导自噬通过整合素/细胞骨架途径促进HepG2细胞的迁移和侵袭。
更新日期:2019-11-01
down
wechat
bug