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ST3Gal III modulates breast cancer cell adhesion and invasion by altering the expression of invasion-related
Hong-Xia Cui1, Honglan Wang1, Yuchun Wang1
1Department of Pharmacology, Qiqihar Medical University, Qiqihar, Heilongjiang 161042, P.R. China.
Abstract:
Changes in the carbohydrate structure on the surface of tumor cells is an important feature of cancer metastasis. The specific role of sialic acids in the glycoconjugate terminal has not yet been clearly elucidated in these processes. Previously, we reported that α2,3-sialic acid residues in breast cancer are associated with metastatic potential. The α2,3-sialyltransferase ST3Gal III, which adds α2,3-sialic acids to glycoproteins, is overexpressed in various tumors, and enzyme activity is correlated with tumor metastasis, yet its mechanistic role has not been fully evaluated. In the present study, we aimed to investigate the influence of ST3Gal III on key steps in the process of breast cancer metastasis. ST3Gal III-overexpressing and ST3Gal III-silenced breast cancer MDA-MB-231 cell lines were generated. They showed an increase or decrease in the tumor-associated antigen sialyl-Lewis X (SLeX). The E-selectin binding capacity of the transfectants was proportional to cell surface SLeX levels. Cell migration and invasion were positively correlated with ST3Gal III levels. Moreover, ST3Gal III expression modulated the protein expression of invasion-related molecules, including β1 integrin, matrix metalloproteinase (MMP)-2, MMP-9 and cyclooxygenase-2, which may account for the mechanism involved in the effects of ST3Gal III on breast cancer invasiveness. In conclusion, our findings in these novel models of ST3Gal III expression revealed a critical requirement for ST3Gal III in several steps of breast cancer metastasis. ST3Gal III modulates breast cancer cell adhesion and invasion by altering the expression of invasion-related molecules. This study provides novel insights into the mechanisms underlying metastasis and suggests a new target for the effective drug treatment of breast cancer metastasis.
Insights
The enzyme ST3Gal III promotes breast cancer metastasis by increasing sialyl-Lewis X (SLeX) on tumor cells. This enhances cell adhesion and invasion, suggesting ST3Gal III as a drug target for treating metastatic breast cancer.
Area of Science:
- Oncology
- Glycobiology
- Molecular Biology
Background:
- Tumor cell surface carbohydrate changes are key in metastasis.
- Sialic acids' role in metastasis is not fully understood.
- α2,3-sialic acid residues correlate with breast cancer metastatic potential.
Purpose of the Study:
- Investigate the influence of α2,3-sialyltransferase (ST3Gal III) on breast cancer metastasis.
- Elucidate the mechanistic role of ST3Gal III in cancer progression.
Main Methods:
- Generated ST3Gal III-overexpressing and -silenced MDA-MB-231 breast cancer cell lines.
- Assessed tumor-associated antigen sialyl-Lewis X (SLeX) expression.
- Measured E-selectin binding, cell migration, and invasion.
- Analyzed protein expression of invasion-related molecules.
Main Results:
- ST3Gal III levels correlated with SLeX expression and E-selectin binding.
- Increased ST3Gal III enhanced cell migration and invasion.
- ST3Gal III modulated expression of β1 integrin, MMP-2, MMP-9, and cyclooxygenase-2.
Conclusions:
- ST3Gal III is critical for multiple steps in breast cancer metastasis.
- ST3Gal III promotes metastasis by altering cell adhesion and invasion-related molecules.
- ST3Gal III represents a potential therapeutic target for breast cancer metastasis.
