Loss of ST3GAL4 exhibits an anticancer effect in breast cancer via the glycolysis pathway

Sialyltransferases responsible for glycoprotein sialylation are key regulators in cancer progression. Although ST3 β‑galactoside α‑2,3‑sialyltransferase 4 (ST3GAL4), an important sialyltransferase, is upregulated in breast cancer, its biological functions remain unclear. The present study aimed to investigate the impact and mechanisms of ST3GAL4 on glycolysis in breast cancer. ST3GAL4 expression was examined in tumor tissue specimens and microarrays and breast cancer cell lines BT‑474, SKBR3, MCF‑7, and T47D. ST3GAL4 was silenced or overexpressed by lentivirus transfection in breast cancer cells. Cell viability and cell cycle were evaluated by Cell Counting Kit‑8 and flow cytometry, respectively. Extracellular acidification rate, glucose uptake and lactate production were used for glycolysis assessment. ST3GAL4 was consistently upregulated in tumor tissues and cell lines of breast cancer. High ST3GAL4 expression was associated with poor prognosis of patients with breast cancer. Cell viability was decreased, cell cycle progression was inhibited and glycolysis was inhibited in ST3GAL4‑silenced cells compared with control cells. ST3GAL4 silencing led to suppression of tumor growth and cell proliferation in xenograft mouse models. ST3GAL4 overexpression promoted cell viability and accelerated cell cycle, which were reversed by glycolysis inhibitor. The study provided in vivo and in vitro evidence that ST3GAL4 promoted cell viability and tumor growth by regulating the glycolysis pathway in breast cancer. ST3GAL4 inhibition may serve as a strategy for treatment of breast cancer.