ArticleGenes to cells : devoted to molecular & cellular mechanisms2025
TIE1 Promotes Primary Tumor Growth by Inhibiting Apoptosis and Activating the AKT-p70S6K Signaling Pathway in Breast Cancer.
Article in Genes to cells : devoted to molecular & cellular mechanisms, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- TIE1 Promotes Primary Tumor Growth by Inhibiting Apoptosis and Activating the AKT-p70S6K Signaling Pathway in Breast Cancer.Genes to cells : devoted to molecular & cellular mechanisms · 2025Article
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Authors and funding
5 authors.
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Abstract
Triple-negative breast cancer (TNBC) is the most aggressive molecular subtype among all breast cancer types. Its treatment remains a significant challenge due to the lack of clearly defined molecular targets. We previously reported that lung-metastatic cell lines, established via orthotopic transplantation of a TNBC cell line, showed high expression of the TIE1 receptor-tyrosine kinase. In this study, we demonstrated that TIE1 expression correlates with poor prognosis in breast cancer patients and is highly elevated in the Claudin-low subtype, which largely overlaps with TNBC. Notably, TIE1 expression promoted tumorigenicity in a breast cancer cell line. Furthermore, in primary tumors formed by TIE1-expressing cells, we observed TIE1 cleavage, reduced apoptosis, and activation of the AKT-p70S6K signaling pathway. Our findings suggest that TIE1 may serve as a potential molecular target and biomarker for Claudin-low type breast cancer, and further research could have significant implications for its treatment.
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