Silencing of integrin subunit a3 inhibits the proliferation, invasion, migration and autophagy of esophageal squamous cell carcinoma cells

被引:5
|
作者
Du, Jin [1 ,2 ]
Zhao, Yang [1 ,2 ]
Hu, Dinghui [1 ,2 ]
Li, Hang [1 ,2 ]
Gao, Lei [1 ,2 ]
Liu, Zuntao [1 ,2 ]
Shi, Kaihu [1 ,2 ]
机构
[1] Nanjing Univ Chinese Med, Affiliated Hosp Integrated Tradit Chinese & Wester, Dept Cardiothorac Surg, Nanjing 210028, Jiangsu, Peoples R China
[2] Jiangsu Prov Acad Tradit Chinese Med, Nanjing 210028, Jiangsu, Peoples R China
关键词
esophageal squamous cell carcinoma; integrin subunit alpha 3; proliferation; invasion; migration; autophagy; CANCER; APOPTOSIS; ITGA3; HEAD;
D O I
10.3892/ol.2022.13391
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Esophageal squamous cell carcinoma (ESCC) is a deadly disease that seriously affects global public health. The aim of the present study was to explore the role of integrin subunit alpha 3 (ITGA3) in ESCC and investigate its detailed molecular mechanisms. Using reverse transcription-quantitative PCR (RT-qPCR) and western blotting, the mRNA and protein expression of ITGA3 in cell lines was detected. In addition, a series of cellular biological experiments, including Cell Counting Kit-8, wound-healing, Transwell and TUNEL assays, were used to evaluate proliferation, migration, invasion and apoptosis, respectively. Furthermore, western blotting was used to measure the expression of corresponding proteins. ITGA3 was found to be upregulated in ESCC cell lines (ECA109 and TE1). It was also found that ITGA3 silencing inhibited the proliferation, migration, invasion and autophagy of ECA109 and TE1 cells but promoted their apoptosis. In addition, ITGA3 silencing was found to inhibit the FAK/PI3K/AKT signaling pathway. In conclusion, ITGA3 knockdown suppressed cell proliferation, invasion, migration and autophagy in ECA109 and TE1 cells, suggesting that ITGA3 may be a potential therapeutic target for the treatment of ESCC.
引用
收藏
页数:8
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