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TRIM11 通过抑制 AMPK 促进非小细胞肺癌细胞的增殖。

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

机构信息

Department of Cardiothoracic Surgery, The Third Hospital of Shijiazhuang, Shijiazhuang, China.

Department of Orthopedics, The Hospital 731, China Aerospace Science and Industry Group, Beijing, China.

出版信息

Clin Respir J. 2023 Oct;17(10):1006-1016. doi: 10.1111/crj.13675. Epub 2023 Aug 21.

Abstract

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.

摘要

肺癌是全球癌症相关死亡的主要原因之一,其中非小细胞肺癌(NSCLC)最为常见。本研究探讨了 TRIM11 基因在 NSCLC 中的作用及其潜在机制。我们从医院招募了 NSCLC 患者,结果显示其 TRIM11 mRNA 和蛋白表达上调。TRIM11 高表达的患者生存率较低。研究发现,TRIM11 基因促进 NSCLC 细胞增殖并减少 ROS 诱导的铁死亡。此外,TRIM11 基因诱导 AMPK 表达,其调控影响 TRIM11 对 NSCLC 细胞增殖和铁死亡的作用。IP 分析显示,TRIM11 蛋白在 NSCLC 中与 AMPK 蛋白相互作用。这些数据证实,TRIM11 通过 AMPK 促进 NSCLC 细胞增殖并减少 ROS 诱导的铁死亡。因此,TRIM11 是治疗 NSCLC 和其他癌症的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ae9/10542972/c022640a0b0c/CRJ-17-1006-g004.jpg

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