Stromal antigen 2 functions as a tumor suppressor in bladder cancer cells

• DOI: 10.3892/or.2017.5711
• Publication Date: 2017-06-12T09:24:58Z
• Authors: Han Wang; Jianhua Zhong; Chenglong Wu; Yang Liu; Jinghua Zhang; Xiaowen Zou; Yan Chen; Jinfeng Su; Gang Yang; Yuantang Zhong; Aifa Tang
• Keywords: Male; 0301 basic medicine; Caspase 3; Tumor Suppressor Proteins; Antigens, Nuclear; Cell Cycle Proteins; Middle Aged; Cadherins; 3. Good health; Gene Expression Regulation, Neoplastic; 03 medical and health sciences; Matrix Metalloproteinase 9; Urinary Bladder Neoplasms; Cell Movement; Biomarkers, Tumor; Humans; Matrix Metalloproteinase 2; Female; Neoplasm Invasiveness; Aged; Cell Proliferation; Neoplasm Staging

Stromal antigen 2 (STAG2) is a subunit of the cohesion complex that plays an important role in the normal segregation of sister chromatids during mitosis or meiosis. However, the effect of STAG2 on the bladder cancer cell proliferation, migration, and invasion has not yet been fully clarified. In this study, we aimed to characterize STAG2 expression and functional significance in BC and adjacent normal tissue. Notably, STAG2 expression was markedly lower in BC cells and tumor tissues than their normal counterparts at the gene and protein levels. Moreover, clinicopathological analysis showed that the low STAG2 expression is associated with TNM stage. Functional analysis demonstrated that STAG2 overexpression attenuated cell proliferation via G1-phase arrest, invasion, and migration, and promoted apoptosis in BC cell lines, while the opposite was observed with STAG2 knockdown cells. Furthermore, STAG2 overexpression upregulated E-cadherin, caspase-3, and caspase-7 and downregulated vimentin, matrix metalloproteinase (MMP)2, and MMP9. Collectively, these data suggest that STAG2 acts as a tumor suppressor gene in bladder cancer and may be a potential therapeutic target in BC.