ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
YB-1 drives triple-negative breast cancer progression and paclitaxel resistance through Wnt/β-catenin pathway.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. 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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1 citing paper in PubMed.
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4 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC) is a highly aggressive and heterogeneous subtype of breast cancer. While chemotherapy remains the cornerstone of TNBC treatment, the frequent development of drug resistance often results in unfavorable clinical outcomes. Y-box binding protein-1 (YB-1) has been implicated in cancer progression and drug resistance, but its specific role and mechanisms in TNBC are poorly understood. This study investigates the impact of YB-1 on TNBC progression and paclitaxel resistance. Tumor and adjacent normal tissues were collected from 10 patients with TNBC to evaluate YB-1 expression. Cell viability, proliferation, and apoptosis were assessed using the CCK-8 assay, EdU staining, and flow cytometry, respectively. A xenograft model was employed to monitor tumor growth, while protein levels were analyzed using western blotting and immunohistochemistry. Elevated YB-1 expression was observed in TNBC tissues and cells. Functional assays revealed that YB-1 overexpression enhanced TNBC cell proliferation, inhibited apoptosis, and heightened resistance to paclitaxel in vitro. Conversely, YB-1 suppression yielded the opposite effects. Mechanistically, YB-1 overexpression was associated with enhanced Wnt/β-catenin pathway activity, which functionally contributed to increased paclitaxel resistance. Similar effects were confirmed in vivo, where YB-1 overexpression accelerated tumor growth, increased paclitaxel resistance, and activated the Wnt/β-catenin pathway, whereas YB-1 suppression reversed these outcomes. In conclusion, YB-1 facilitates TNBC cell proliferation, suppresses apoptosis, and strengthens paclitaxel resistance through activation of the Wnt/β-catenin pathway. These findings highlight YB-1 as a promising therapeutic target for TNBC treatment.
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