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

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

doi:10.7150/jca.86511

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J Cancer 2024; 15(11):3394-3405. doi:10.7150/jca.86511 This issue Cite

Research Paper

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

Yini Cai^1#, Jiali Zhao^1#, Chen Luo¹, Ming Fang³, Yanling Yi¹, Yu Chen¹, Peng Huang¹, Lingmin Liao^2✉, Long Huang^1✉

1. 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.
2. Department of Ultrasound, The Second Affiliated Hospital, JiangXi Medical College, Nanchang University, Nanchang, China.
3. Department of Yangxin People's Hospital of Hubei Province, 81 Ruxue Road, Xingguo Town, Yangxin County, Huangshi, Hubei, China.
#The first authors with equal contributions.

Citation:

Cai Y, Zhao J, Luo C, Fang M, Yi Y, Chen Y, Huang P, Liao L, Huang L. CD52 knockdown inhibits aerobic glycolysis and malignant behavior of NSCLC cells through AKT signaling pathway. J Cancer 2024; 15(11):3394-3405. doi:10.7150/jca.86511. https://www.jcancer.org/v15p3394.htm

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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 in vitro and in vivo. 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.

Keywords: NSCLC, CD52, Proliferation, Migration, aerobic glycolysis, AKT

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APA

Cai, Y., Zhao, J., Luo, C., Fang, M., Yi, Y., Chen, Y., Huang, P., Liao, L., Huang, L. (2024). CD52 knockdown inhibits aerobic glycolysis and malignant behavior of NSCLC cells through AKT signaling pathway. Journal of Cancer, 15(11), 3394-3405. https://doi.org/10.7150/jca.86511.

ACS

Cai, Y.; Zhao, J.; Luo, C.; Fang, M.; Yi, Y.; Chen, Y.; Huang, P.; Liao, L.; Huang, L. CD52 knockdown inhibits aerobic glycolysis and malignant behavior of NSCLC cells through AKT signaling pathway. J. Cancer 2024, 15 (11), 3394-3405. DOI: 10.7150/jca.86511.

NLM

CSE

Cai Y, Zhao J, Luo C, Fang M, Yi Y, Chen Y, Huang P, Liao L, Huang L. 2024. CD52 knockdown inhibits aerobic glycolysis and malignant behavior of NSCLC cells through AKT signaling pathway. J Cancer. 15(11):3394-3405.

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