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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Adult, Aged, Aged, 80 and over, Animals, Cell Line, Tumor, Female, Gene Expression Regulation, Neoplastic, Humans, Male, Mice, Middle Aged, Neoplasm Transplantation, Neovascularization, Pathologic, Prognosis, Sp1 Transcription Factor, Sp2 Transcription Factor, Stomach Neoplasms, Sulfotransferases, Up-Regulation, Vascular Endothelial Growth Factor A.
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Does overexpression of SULT2B1b promote Angiogenesis in Human Gastric Cancer? Context: Overexpression of cytosolic sulfotransferase 2B1b (SULT2B1b) has been commonly found in colorectal and hepatocellular carcinoma, suggesting that SULT2B1b might act as a potential oncogenic protein. However, its clinical significance and biological role in gastric cancer progression remain largely unknown. Expressions of SULT2B1b in clinical gastric cancer (GC) samples were examined using qRT-PCR and Western blot. SULT2B1b was markedly overexpressed in human GC samples, and positively correlated with vessel density and associated with poor clinical features. We also demonstrated that overexpression of SULT2B1b resulted in increased tumor angiogenesis and tumor growth in mouse GC models. In addition, ablation of SULT2B1b in human GC cells lines BGC823 and MKN45 decreased the capability of the cells to recruit endothelial cells. Moreover, depletion of SULT2B1b in GC cells reduced VEGF-A expression by downregulating SP1 and AP2.
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Our results suggested that the SULT2B1b-mediated angiogenic pathway could serve as biomarkers for GC diagnosis and prognosis, and suppressing SULT2B1b-mediated angiogenic signaling might be a promising strategy for developing novel GC treatment. Final Decision: yes