TGFB Induced Factor Homeobox 2 Induces Deterioration of Bladder Carcinoma via Activating CD2 Cytoplasmic Tail Binding Protein 2

Abstract

Bladder carcinoma is a complex and aggressive malignancy with limited treatment options. In this study, we aimed to investigate the expression pattern of TGIF2 in bladder carcinoma and its clinical significance, as well as its functional role and interaction with CD2BP2 in disease progression. Through quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analysis, we found that TGIF2 was highly expressed in bladder carcinoma tissues compared to normal bladder mucosa. Furthermore, elevated TGIF2 levels were associated with advanced tumor stage and larger tumor size, indicating its potential as a prognostic marker in bladder carcinoma. Using knockdown models in bladder carcinoma cell lines (253j and J82), we observed that the inhibition of TGIF2 resulted in decreased proliferation and migration rates, suggesting a critical role of TGIF2 in promoting these malignant phenotypes. Additionally, our dual-luciferase reporter assay revealed a direct interaction between TGIF2 and CD2BP2, with CD2BP2 being upregulated in bladder carcinoma tissues and positively correlated with TGIF2 expression. Notably, the overexpression of CD2BP2 reversed the suppressed malignant phenotypes caused by TGIF2 knockdown. Collectively, our findings highlight the abundant expression of TGIF2 in bladder carcinoma tissues and its association with malignant characteristics. We demonstrate that TGIF2 promotes proliferative and metastatic capacities in bladder carcinoma by positively regulating CD2BP2. These insights provide a basis for further investigations into the potential of TGIF2 and CD2BP2 as therapeutic targets and prognostic markers in bladder carcinoma management.