B3GALT4 modulates tumor progression and autophagy by AKT/mTOR signaling pathway in breast cancer
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Updated: Jun 11, 2025
Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
Published on: June 9, 2023
Yongliang Sha1, Huijie Zhuang1, Jin Shi1
1Department of General Surgery, Xuzhou Central Hospital, 199 Jiefang South Road, Xuzhou, 221009, Jiangsu, China.
Background:
β-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.
Method:
Publically 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.
Results:
B3GALT4 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.
Conclusion:
According 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.
Insights
Beta-1,3-galactosyltransferase-4 (B3GALT4) promotes breast cancer growth by inhibiting autophagy through the AKT/mTOR pathway. Targeting B3GALT4 may offer a new therapeutic strategy for breast cancer patients.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Beta-1,3-galactosyltransferase-4 (B3GALT4) is implicated in various cancers.
- Its specific role in breast cancer pathogenesis remains largely uncharacterized.
Purpose of the Study:
- To investigate the expression and function of B3GALT4 in breast cancer.
- To explore the underlying molecular mechanisms, including its effect on autophagy and the AKT/mTOR pathway.
Main Methods:
- Analysis of public datasets and patient samples using qPCR, western blot, and immunohistochemistry.
- In vitro and in vivo studies to assess the impact of B3GALT4 on cancer cell behavior.
- Investigation of autophagy markers (LC3) and the AKT/mTOR pathway via RNA-seq and western blot.
Main Results:
- B3GALT4 is overexpressed in breast cancer and correlates with poor prognosis.
- B3GALT4 overexpression enhances tumor cell proliferation, migration, and invasion.
- Inhibition of B3GALT4 suppresses tumor growth and triggers autophagy by hindering the AKT/mTOR pathway.
Conclusions:
- B3GALT4 promotes breast cancer progression by suppressing autophagy via the AKT/mTOR signaling pathway.
- B3GALT4 represents a potential therapeutic target for breast cancer treatment.
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