ST6GAL1 Promotes Epithelial-to-Mesenchymal Transition in Breast Cancer via the HIF-HK2 Signaling Pathway

Breast cancer presents a substantial clinical challenge because of its complex aetiology and diverse phenotypic presentations. ST6Gal1 expression and epithelial-to-mesenchymal transition (EMT) frequently lead to metastasis, drug resistance and poor prognosis in many cancers. Nevertheless, the molecular details surrounding ST6GAL1 in the carcinogenesis of breast cancer, especially in the EMT of breast cancer, remain unclear. The objective of this study was to clarify the possible role and mechanism of ST6GAL1 in breast cancer.

PCR, WB, and IHC were employed to analyze the expression of ST6GAL1, epithelial-mesenchymal transition (EMT) markers, and components of the HIF-HK2 signaling pathway in MCF-10A, MDA-MB-231, and MCF-7 cells. Wound-healing, cell adhesion, drug resistance and extracellular matrix invasion assays were used to analyse the effects of ST6GAL1 on the biological process of breast cancer cells. The HIF-HK2 signalling pathway was also analysed.

ST6GAL1 expression is increased in breast cancer. Altered expression of ST6GAL1 affects the biological function of breast cancer cells both in vitro and in vivo. ST6GAL1 knockdown inhibited EMT in breast cancer cells. ST6GAL1 Mediates the Activity of the HIF-HK2 Signalling Pathway in Breast Carcinoma Cells.

In our study, in vitro and in vivo models revealed that ST6GAL1 promotes malignant phenotypes in breast cancer cells and regulates the EMT process through activation of the HIF-HK2 signalling pathway.