OncoTargets and Therapy (Jan 2020)
ST6GAL2 Downregulation Inhibits Cell Adhesion and Invasion and is Associated with Improved Patient Survival in Breast Cancer
Abstract
Junchi Cheng,1,* Rong Wang,1,* Guansheng Zhong,2 Xi Chen,1 Yun Cheng,1 Wei Li,1 Yunshan Yang1 1Department of Medical Oncology, Cancer Hospital of the University of Chinese Academy of Sciences, Hangzhou 310000, People’s Republic of China; 2Department of Breast Surgery, The First Affiliated Hospital, Zhejiang University, Hangzhou 310003, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yunshan YangDepartment of Medical Oncology, Cancer Hospital of the University of Chinese Academy of Sciences, 1st Banshandong Road, Hangzhou 310000, People’s Republic of ChinaTel +86-57188122052Email [email protected]: 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.Keywords: breast cancer, ST6GAL2, prognosis, adhesion, invasion
