The Journal of Practical Medicine ›› 2024, Vol. 40 ›› Issue (1): 13-18.doi: 10.3969/j.issn.1006-5725.2024.01.003

• Feature Reports:Lung cancer • Previous Articles     Next Articles

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

Xue MA,Shihui. ZHOU()   

  1. Department of Emergency,the First Affiliated Hospital of Jinzhou Medical University,Jinzhou 121001,China
  • Received:2023-10-01 Online:2024-01-10 Published:2024-01-24
  • Contact: Shihui. ZHOU E-mail:1060402586@qq.com

Abstract:

Objective To investigate the effect and regulatory mechanism of autophagy related multifunctional 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 addition, 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 modulating autophagy.

Key words: non?small cell lung cancer, autophagy, proliferation, migration, invasion

CLC Number: