ArticleDiscover oncology2024
B3GALT4 modulates tumor progression and autophagy by AKT/mTOR signaling pathway in breast cancer.
Article in Discover oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Integrative machine learning and multi-omics identify a centromere gene signature and validate B3GALT4 as a tumor suppressor in osteosarcoma.Journal of bone oncology · 2026Article
- A novel model for assessing lymph node metastasis and the immune microenvironment in breast cancer by integrating digital pathology images and transcriptomics.Discover oncology · 2026Article
- Ultrasound-based radiomics combined with B3GALT4 level to predict sentinel lymph node metastasis in primary breast cancer.Frontiers in oncology · 2025Article
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9 authors.
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Abstract
backgroundβ-1,3-Galactosyltransferase-4 (B3GALT4), a member of the β-1,3-galactosyltransferase gene family, is essential to the development of many malignancies. However, its biological function in breast cancer is still unknown.
methodPublically accessible datasets, as well as quantitative real-time PCR, western blot, and immunohistochemistry on our patient cohort were used to investigate the expression levels of B3GALT4 in breast cancer. The correlation of B3GALT4 expression with clinical histopathological data and mortality in breast cancer patients was investigated. The effects of B3GALT4 in breast cancer in vitro and in vivo were investigated. RNA-seq, western blot, autophagolysosomes, and the fluorescence intensity of LC3 were used to explore the effects of B3GALT4 on autophagy. Western blot and gene set enrichment analysis (GSEA) were used to identify the AKT/mTOR pathway.
resultsB3GALT4 was significantly overexpressed in breast cancer tissues and was positively correlated with some aspects of clinicopathological status and poor prognosis. B3GALT4 overexpression significantly promoted cell proliferation, migration, and invasion, both in vitro and in vivo. B3GALT4 inhibition suppressed breast cancer cell proliferation, migration, and invasion in vitro. Suppression of B3GALT4 triggered autophagy and hindered the AKT/mTOR signaling pathway.
conclusionAccording to the present research, B3GALT4 blocked autophagy via the AKT/mTOR pathway and accelerated the growth of breast cancer. B3GALT4 may be an effective target for patients with breast cancer.
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