TRIM11 promotes cell proliferation of non-small cell lung cancer through the inhibition of ferroptosis by AMPK

被引:2
|
作者
Liang, Zheng [1 ]
Li, Jian [2 ]
Zhang, Guoliang [1 ]
Chen, Menghui [1 ]
机构
[1] Third Hosp Shijiazhuang, Dept Cardiothorac Surg, 15 South Sports St, Shijiazhuang 050000, Hebei, Peoples R China
[2] China Aerosp Sci & Ind Grp, Hosp 731, Dept Orthoped, Beijing, Peoples R China
来源
CLINICAL RESPIRATORY JOURNAL | 2023年 / 17卷 / 10期
关键词
AMPK; ferroptosis; non-small cell lung cancer; TRIM11;
D O I
10.1111/crj.13675
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
Lung cancer is one of the leading causes of cancer-related deaths worldwide, with non-small cell lung cancer (NSCLC) being the most prevalent type. This study investigates the role of TRIM11 gene in NSCLC and its underlying mechanism. NSCLC patients were recruited from our hospital and showed upregulated TRIM11 mRNA and protein expressions. Patients with high TRIM11 expression had lower survival rates. TRIM11 gene was found to promote cell proliferation and reduce ROS-induced ferroptosis in NSCLC. Additionally, TRIM11 gene induced AMPK expression and its regulation affected TRIM11's effects on cell proliferation and ferroptosis in NSCLC. IP analysis revealed that TRIM11 protein interacted with AMPK protein in NSCLC. These data confirmed that TRIM11 promotes cell proliferation and reduces ROS-induced ferroptosis in NSCLC through AMPK. Hence, TRIM11 is a potential target for the treatment of NSCLC and other cancers.
引用
收藏
页码:1006 / 1016
页数:11
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