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SOS1 regulates HCC cell epithelial-mesenchymal transition via the PI3K/AKT/mTOR pathway

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资源类型：
Pubmed体系：
作者：
Li Yonghe[1,2] * ; Yin Yaolin[1,2] ; He Yi[1,2] ; He Kun[1,2] ; Li Jingdong[1,2,*1] ;
机构： [1]Department of Hepatobiliary Surgery, Affiliated Hospital of North Sichuan Medical College, Nanchong, China [2]Institute of Hepato-Biliary-Pancreatic-Intestinal Disease, North Sichuan Medical College, Nanchong, China
出处：
DOI： 10.1016/j.bbrc.2022.11.015
ISSN：

关键词： SOS1 Epithelial-mesenchymal-transition Hepatocellular carcinoma PI3K/AKT/mTOR

摘要：
The influence of son of sevenless homolog 1 (SOS1) on invasion and metastasis of hepatocellular carcinoma (HCC) cells was investigated. HCC cells were transfected with siRNA and lentivirus to achieve SOS1 knock down/overexpression and changes in RNA and protein levels analyzed by q-PCR and Western blotting (WB). Transwell assay was utilized to assess variations in cell invasion and migration in vitro and by a lung metastasis model of liver cancer in vivo. High expression of SOS1 was observed in most human liver cancers, which indicated a worse prognosis. SOS1 knockout in HepG2 cells significantly decreased cell invasion and migration. SOS1 knockout also reduced the number of metastatic foci in a lung metastasis model of HCC established in nude mice. SOS1 knockout inhibited the epithelial-mesenchymal transition (EMT) in HepG2 cells as well as the PI3K/AKT/mTOR pathway. Overexpression of SOS1 in Huh7 cells had the opposite effect. To conclude, SOS1 may induce the EMT by the activation of the PI3K/AKT/mTOR pathway, thereby enhancing invasion, migration and metastasis of HCC cells. These findings may expose SOS1 as a new HCC therapeutic target.Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.

基金：
National Health Commission of China (NO. WA2021RW26); Scientific Research Project of Sichuan Provincial Health Commission (NO.20PJ149); and Nanchong Municipal School Science and Technology Strategic Cooperation Project (NO.18SXHZ0186).
语种：
外文
PubmedID：
中科院(CAS)分区：
出版当年[2022]版：
大类 | 4 区 生物学
小类 | 4 区 生化与分子生物学 4 区 生物物理
最新[2023]版：
大类 | 3 区 生物学
小类 | 3 区 生物物理 4 区 生化与分子生物学
第一作者：
第一作者机构： [1]Department of Hepatobiliary Surgery, Affiliated Hospital of North Sichuan Medical College, Nanchong, China [2]Institute of Hepato-Biliary-Pancreatic-Intestinal Disease, North Sichuan Medical College, Nanchong, China
通讯作者：
通讯机构： [1]Department of Hepatobiliary Surgery, Affiliated Hospital of North Sichuan Medical College, Nanchong, China [2]Institute of Hepato-Biliary-Pancreatic-Intestinal Disease, North Sichuan Medical College, Nanchong, China [*1]Department of Hepatobiliary Surgery, Affiliated Hospital of North Sichuan Medical College, Nanchong, China.
推荐引用方式(GB/T 7714)：
Li Yonghe,Yin Yaolin,He Yi,et al.SOS1 regulates HCC cell epithelial-mesenchymal transition via the PI3K/AKT/mTOR pathway[J].Biochemical and biophysical research communications.2022,637:161-169.doi:10.1016/j.bbrc.2022.11.015.
APA：
Li Yonghe,Yin Yaolin,He Yi,He Kun&Li Jingdong.(2022).SOS1 regulates HCC cell epithelial-mesenchymal transition via the PI3K/AKT/mTOR pathway.Biochemical and biophysical research communications,637,
MLA：
Li Yonghe,et al."SOS1 regulates HCC cell epithelial-mesenchymal transition via the PI3K/AKT/mTOR pathway".Biochemical and biophysical research communications 637.(2022):161-169

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