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p62/SQSTM1在非小细胞肺癌细胞增殖和侵袭转移中的作用

马雪 周世辉

实用医学杂志2024,Vol.40Issue(1):13-18,6.
实用医学杂志2024,Vol.40Issue(1):13-18,6.DOI:10.3969/j.issn.1006-5725.2024.01.003

p62/SQSTM1在非小细胞肺癌细胞增殖和侵袭转移中的作用

Role and potential mechanisms of p62/SQSTM1 on migration and metastasis of non-small cell lung cancer

马雪 1周世辉1

作者信息

  • 1. 锦州医科大学附属第一医院急诊科(辽宁锦州 121001)
  • 折叠

摘要

Abstract

Objective To investigate the effect and regulatory mechanism of autophagy related multifunc-tional protein p62/SQSTM1 on biological behavior in non-small cell lung cancer(NSCLC).Methods RT-qPCR was used to detect the expression of p62 in normal lung cells and NSCLC cells.CCK-8,wound-healing and Transwell assays were used to detect the effects of inhibition and promotion of p62 expression on the proliferation,migration and invasion in NSCLC cells.Western blotting was used to detect the effects of inhibition and promotion of p62 expression on the expression of apoptosis-related proteins(Bcl-2 and Bax)and autophagy-related proteins(ATG5 and Becline1)in NSCLC cells.A nude mouse transplantation tumor experiment was used to detect the effect of inhibiting p62 expression on the tumor volume and mass of NSCLC cells in vivo.Results Compared with that in normal lung cells,the expression level of p62 in A549 cells was the highest.Cell function experiments in vitro showed that inhibition of p62 expression reduced the abilities of proliferation,migration and invasion in A549 cells,and suppressed autophagy and induced apoptosis.Consistently,p62 overexpression has the opposite effects.In addi-tion,animal experiments in vivo showed that inhibition of p62 expression decreased the tumor volume and mass of tumor-bearing mice.Conclusion p62 could promote the growth of NSCLC A549 cell in vivo and in vitro by modu-lating autophagy.

关键词

非小细胞肺癌/p62/自噬/增殖/迁移/侵袭

Key words

non-small cell lung cancer/autophagy/proliferation/migration/invasion

分类

医药卫生

引用本文复制引用

马雪,周世辉..p62/SQSTM1在非小细胞肺癌细胞增殖和侵袭转移中的作用[J].实用医学杂志,2024,40(1):13-18,6.

基金项目

辽宁省科技计划项目(编号:2022-MS-21) (编号:2022-MS-21)

实用医学杂志

OA北大核心CSTPCD

1006-5725

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