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Updated: Feb 28, 2026

Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
Published on: October 30, 2013
Stromal antigen 2 functions as a tumor suppressor in bladder cancer cells
Han Wang1, Jianhua Zhong2, Chenglong Wu3
1Shenzhen Second People's Hospital, Clinical Medicine College of Anhui Medical University, Shenzhen, Guangdong 518039, P.R. China.
Abstract:
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.
Insights
Stromal antigen 2 (STAG2) is downregulated in bladder cancer (BC). Overexpression of STAG2 inhibits BC cell proliferation, invasion, and migration, suggesting it acts as a tumor suppressor.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Stromal antigen 2 (STAG2) is a key component of the cohesion complex, crucial for sister chromatid segregation during cell division.
- The precise role of STAG2 in bladder cancer (BC) progression, including its effects on cell proliferation, migration, and invasion, remains incompletely understood.
Purpose of the Study:
- To investigate the expression levels of STAG2 in bladder cancer tissues and cells compared to normal tissues.
- To elucidate the functional significance of STAG2 in regulating bladder cancer cell behavior, including proliferation, apoptosis, invasion, and migration.
Main Methods:
- Quantitative analysis of STAG2 gene and protein expression in BC and adjacent normal tissues.
- In vitro functional assays involving STAG2 overexpression and knockdown in BC cell lines to assess effects on cell cycle, apoptosis, invasion, and migration.
- Western blot analysis to evaluate the expression of key proteins involved in cell adhesion, apoptosis, and metastasis.
Main Results:
- STAG2 expression was significantly lower in BC cells and tumor tissues compared to normal counterparts at both gene and protein levels.
- Low STAG2 expression correlated with advanced TNM stage in bladder cancer patients.
- STAG2 overexpression suppressed BC cell proliferation (via G1 arrest), invasion, and migration, while promoting apoptosis.
- STAG2 overexpression led to increased E-cadherin, caspase-3, and caspase-7, and decreased vimentin, MMP2, and MMP9.
Conclusions:
- STAG2 functions as a tumor suppressor gene in bladder cancer.
- STAG2 downregulation is associated with BC progression and adverse clinicopathological features.
- STAG2 represents a potential therapeutic target for bladder cancer treatment.
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