<p>ST6GAL2 Downregulation Inhibits Cell Adhesion and Invasion and is Associated with Improved Patient Survival in Breast Cancer</p>

Abstract

These authors contributed equally to this workObjective: Breast cancer is one of the most common and serious types of cancer, with a particularly unfavorable prognosis. Although dysregulation of β-galactoside α 2,6-sialyltransferase 2 (ST6GAL2) has been observed in multiple cancers, the mechanism involved remains to be clarified. In this study, we focused on the potential function of ST6GAL2 in the regulation of breast cancer. Methods: Flow cytometry and CCK-8 were used to measure markers of the cell cycle proliferation, adhesion, and invasion. Real-time PCR and immunohistochemistry analysis were used to detect the expression levels of ST6GAL2 in breast cancer tissues. Western blot was used to analyze the expression level of genes correlated with focal adhesion and metastasis pathways in breast cancer cells. Results: ST6GAL2 expression levels were higher in breast cancer tissues as compared to healthy tissues. ST6GAL2 expression was associated with tumor stage, survival time, and estrogen receptor (ER)/progesterone receptor (PR)/human epidermal growth factor receptor 2 (HER2) status of breast cancer patients. Silence of ST6GAL2 inhibited cancer progression by arresting cell cycle progression at G0/G1 phase and inhibiting cell adhesion and invasion. ST6GAL2 was positively correlated with focal adhesion and metastasis pathways, and its downregulation inhibited the expression of ICAM-1, VCAM-1, CD24, MMP2, MMP9, and CXCR4. Conclusion: These findings indicated that ST6GAL2 might serve as a useful potential target for treatment of breast cancer.

Siglec‐15 promotes the migration of liver cancer cells by repressing lysosomal degradation of CD44

“…We examined whether inhibiting sialylation influenced the effect of Siglec‐15 on HCC cells. β‐galactoside α‐2,6‐sialyltransferase 1(ST6GAL1) is a sialyltransferase that catalyzes the sialic acid residues to terminal galactose of glycan chains by α 2,6‐sialylation [22].…”

Investigation of the miRNA and mRNA Coexpression Network and Their Prognostic Value in Hepatocellular Carcinoma

“…Thus, the effect of miR-324-5P on tumor progression might be different via different mechanisms. Among target genes, the high expression of alpha-2,6-sialyltransferase 2 (ST6GAL2), one of the top 100 of all the 1236 downregulated genes, was demonstrated to promote tumorigenesis of follicular thyroid cancer via activating the Hippo signaling pathway [ 30 ], and the downregulation of ST6GAL2 is associated with improved patient survival in breast cancer [ 31 ], but the effects of ST6GAL2 have not been reported yet on the oncogenesis and the progression of HCC. Regulator of calcineurin 1(RCAN1) is broadly expressed in the liver, placenta, and other tissues.…”

Aberrant Sialylation in Cancer: Biomarker and Potential Target for Therapeutic Intervention?

“…In a study of 633 breast cancer patients, ST6GAL1 expression was associated with tumor stage, survival and estrogen receptor (ER)/progesterone receptor (PR)/human epidermal growth factor receptor 2 (HER2) status. Consistently, silencing of ST6GAL2 negatively affected cancer progression by inhibiting cell adhesion and invasion, and reducing the expression of ICAM-1, VCAM-1, CD24, MMP2, MMP9, and CXCR4 [ 43 ].…”

“…ST6GAL1 silencing attenuated proliferation and colony formation ability of PC-3 and DU145 prostate cancer cell lines, through inhibition of the PI3K/AKT/GSK-3β/β-catenin pathway [ 42 ]. Similarly, ST6GAL2 silencing inhibited MCF-7 and T47D breast cancer cell proliferation by arresting cell cycle progression at G0/G1 phase and reducing the fraction of cells in S phase [ 43 ].…”