ArticleBreast cancer (Dove Medical Press)2025
HGH1 Promotes Breast Cancer Progression Through the PI3K/AKT/NF-κB Signaling Pathway: Potential Role for Prognosis and Targeted Therapy.
Article in Breast cancer (Dove Medical Press), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- The role of growth hormone in metastasis and angiogenesis of breast cancer.Bioscience reports · 2026Review
- Cellular senescence in cancer: from mechanism paradoxes to precision therapeutics.Molecular cancer · 2025Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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