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CD52基因敲低通过AKT信号通路抑制非小细胞肺癌细胞的有氧糖酵解和恶性行为。

CD52 knockdown inhibits aerobic glycolysis and malignant behavior of NSCLC cells through AKT signaling pathway.

作者信息

Cai Yini, Zhao Jiali, Luo Chen, Fang Ming, Yi Yanling, Chen Yu, Huang Peng, Liao Lingmin, Huang Long

机构信息

Department of Oncology, The Second Affiliated Hospital of Nanchang University; Jiangxi Key Laboratory of Clinical and Translational Cancer Research, 1 Minde Road, Nanchang, Jiangxi, China.

Department of Yangxin People's Hospital of Hubei Province, 81 Ruxue Road, Xingguo Town, Yangxin County, Huangshi, Hubei, China.

出版信息

J Cancer. 2024 Apr 29;15(11):3394-3405. doi: 10.7150/jca.86511. eCollection 2024.

DOI:10.7150/jca.86511
PMID:38817869
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11134428/
Abstract

CD52 is an important functional regulator involved in the development of human cancer. In this study, the clinical significance and biological function of CD52 in the malignant behavior of non-small cell lung cancer (NSCLC) were explored. In this study, immunohistochemical (IHC) staining was performed to determine the expression pattern of CD52 in NSCLC. Loss of function assays were used to evaluate the biological functions of CD52 in NSCLC cells and . Our data indicated that the expression of CD52 was significantly elevated in NSCLC and correlated with the patient prognosis. Functionally, downregulation of CD52 expression significantly suppressed the proliferation, migration, aerobic glycolysis and tumorigenesis of NSCLC cells. Moreover, CD52 regulated aerobic glycolysis of NSCLC cells through the AKT pathway. Furthermore, aerobic glycolysis induced by 2-DG inhibited the proliferation of NSCLC cells. In conclusion, CD52 knockdown inhibited aerobic glycolysis and malignant behavior of NSCLC cells through AKT signaling pathway, which may be employed in an alternative therapeutic target for NSCLC.

摘要

CD52是参与人类癌症发展的重要功能调节因子。在本研究中，探讨了CD52在非小细胞肺癌（NSCLC）恶性行为中的临床意义和生物学功能。在本研究中，进行免疫组织化学（IHC）染色以确定CD52在NSCLC中的表达模式。采用功能缺失试验评估CD52在NSCLC细胞中的生物学功能。我们的数据表明，CD52在NSCLC中的表达显著升高，且与患者预后相关。在功能上，CD52表达的下调显著抑制了NSCLC细胞的增殖、迁移、有氧糖酵解和肿瘤发生。此外，CD52通过AKT途径调节NSCLC细胞的有氧糖酵解。此外，2-DG诱导的有氧糖酵解抑制了NSCLC细胞的增殖。总之，CD52基因敲低通过AKT信号通路抑制了NSCLC细胞的有氧糖酵解和恶性行为，这可能成为NSCLC的另一种治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d70a/11134428/34975ad7aea3/jcav15p3394g006.jpg
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