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Archive > Volume 32 Issue 8 > 2025,32(8):847-853. DOI:10.3872/j.issn.1007-385X.2025.08.008 Prev Next
Clinical Research
Expression, function and regulatory mechanisms of dystrobrevin-α in gastric cancer
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Abstract:
[Abstract] Objective: To investigate the expression characteristics, biological functions, and regulatory mechanisms of dystrobrevin-ɑ (DTNA) in gastric cancer tissues. Methods: Bioinformatics analysis based on public databases was used to predict DTNA expression in gastric cancer and its correlation with prognosis. Bioinformatics analysis based on public databases was used to predict DTNA expression in gastric cancer and its correlation with prognosis. qPCR and immunohistochemistry (IHC) were employed to detect DTNA expression in gastric cancer tissues and cells. The chi-square test analyzed the correlations between DTNA and clinicopathological features of gastric cancer, while Kaplan Meier survival analysis assessed the relationship between DTNA expression and prognosis. CCK-8 and Transwell assays detected the effects of DTNA on the proliferation, migration, and invasion of gastric cancer MGC-803 cells. RNA interference, qPCR, and WB assay were used to examine the effects of far upstream element-binding protein 1 (FUBP1) on DTNA expression in MGC-803 cells. Results: Bioinformatics analysis revealed upregulated DTNA expression in gastric cancer tissues versus adjacent tissues, correlating with poor prognosis. DTNA was upregulated in gastric cancer tissues (P < 0.0001) and cells (P < 0.05), showing positive correlations with T stage (P < 0.001), TNM stage (P = 0.001), and poor prognosis (Log-Rank P = 0.0039). DTNA knockdown significantly inhibited the proliferation, migration, and invasion abilities of MGC-803 cells (all P < 0.01). FUBP1 downregulation reduced DTNA expression (P < 0.01). Conclusion: DTNA is upregulated in gastric cancer tissues and cells and is correlated with disease progression and poor prognosis. DTNA knockdown inhibits the proliferation, migration, and invasion of gastric cancer cells, and its expression is regulated by FUBP1.
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