Effects of LAIR‐1 on hepatocellular carcinoma cell proliferation and invasion via PI3K‐AKT‐mTOR pathway regulation

Author:

Zhou Ti1,Liu Luqing2,Lan Haibin1,Fang Donglin1ORCID

Affiliation:

1. Department of General Surgery The First People's Hospital of Lin ping District Hangzhou Zhejiang China

2. Department of General Surgery The People's Hospital of Guannan County Lianyungang Jiangsu China

Abstract

AbstractIntroductionHepatocellular carcinoma (HCC) is one of the common malignant tumors. Although surgical resection is the best treatment for HCC, many patients with HCC are found to have metastases at the time of initial diagnosis and lose the opportunity for radical treatment. Therefore, the study of the invasion and metastasis of HCC has always been the focus of HCC research. This study aimed to assess the influence of LAIR‐1 on HCC cell proliferation and invasion and the relevant mechanisms involved in this process.MethodsImmunocytochemical staining assay, quantitative real‐time polymerase chain reaction (qRT‐PCR) and western blotting (WB) were used to detect the expression of LAIR‐1mRNA and protein in healthy human hepatocyte LO2 and the HCC cell lines HepG2, Bel‐7402, MHCC97‐H, and Huh‐7. Then, we evaluated the cell viability, colony formation, and invasion of MHCC97‐H and Huh‐7 cells in each group by silencing or overexpressing LAIR‐1 expression in MHCC97‐H and Huh‐7 cells, respectively. WB was used to detect the expression levels of PI3K‐AKT‐mTOR pathway related proteins.ResultsOur findings showed that LAIR‐1 can inhibit cell viability, colony formation and invasion in vitro. Meanwhile, LAIR‐1 significantly downregulated the expression of PI3K, p‐AKT and p‐mTOR, which were abolished by the PI3K inhibitor, LY294002.ConclusionsOur study revealed that LAIR‐1 inhibited cell proliferation and invasion, probably via suppressing the PI3K‐AKT‐mTOR pathway.

Publisher

Wiley

Subject

Immunology,Immunology and Allergy

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3