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HGH1 顺利获得 PI3K/AKT/NF-κB 信号通路促进乳腺癌进展:对预后及靶向治疗的潜在作用
Authors Hu W, Si D, Liu C, Tie D, Xu D, Li N
Received 8 November 2024
Accepted for publication 28 March 2025
Published 14 April 2025 Volume 2025:17 Pages 325—337
DOI http://doi.org/10.2147/BCTT.S505492
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Professor Pranela Rameshwar
Wenyu Hu,1,* Dikun Si,1,* Chenxi Liu,2,* Danchen Tie,1 Dongdong Xu,1 Nanlin Li1
1Department of Thyroid, Breast and Vascular Surgery, Xijing Hospital, Air Force Medical University, Xi’an, Shaanxi, People’s Republic of China; 2Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Nanlin Li, Email nanlin-74@163.com
Introduction: Previous studies have shown that the HGH1 gene is associated with poor prognosis in a variety of cancers, but its specific function and molecular mechanism in the pathological process of breast cancer remain unclear.
Methods: The relationship between expression of HGH1 and overall survival in BC patients was analyzed. Enrichment analysis of HGH1-related signaling pathways and immune infiltration was performed. BC cell lines with overexpression and knockdown of HGH1 gene were constructed to tested the proliferation, migration, invasion ability and cell apoptosis. Detected the expression of PI3K/AKT pathway in BC cells and treated it with PI3K inhibitor. The effect of HGH1 on breast cancer in vivo was observed by tumor xenograft experiment.
Results: The expression of HGH1 is significantly increased in breast cancer and related to poor prognosis. The high expression of HGH1 is related to the PI3K−Akt signaling pathway, cell cycle, cell senescence, P53 signaling pathway. Overexpression of HGH1 promotes the proliferation, migration, and invasion, and inhibits apoptosis, while its knockdown yields opposite effects. HGH1 promoted the growth of BC cells by activating the PI3K/AKT/NF-κB signaling pathway, and the use of PI3K inhibitors could attenuate the promoting effect. In vivo experiments confirmed that HGH1 promoted breast cancer growth.
Conclusion: HGH1 promotes the growth of BC cells by activating the PI3K/AKT/NF-κB signaling pathway. HGH1 may become a new indicator for evaluating the poor prognosis of BC patients and serve as a potential diagnostic biomarker and therapeutic target for breast cancer.
Keywords: breast cancer, HGH1, PI3K, circadian