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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: Animals, Apoptosis, Biomarkers, Tumor, Blotting, Western, Cell Line, Tumor, Cell Survival, Female, Flow Cytometry, Gene Expression Regulation, Neoplastic, Gene Knockdown Techniques, Humans, Mice, Mice, Inbred BALB C, Mice, Nude, Neuroblastoma, Phenotype, RNA Interference, Random Allocation, Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, beta Catenin.
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Does knockdown of β-catenin expression inhibit neuroblastoma cell growth in vitro and in vivo? Context: The purpose of this study was to investigate the inhibitory effect of β-catenin gene silencing on regulation of the biological behavior of neuroblastoma BE(2)C cells in vivo and in vitro. A lentivirus, carrying β-catenin siRNA, was used to stably knockdown β-catenin expression in neuroblastoma BE(2)C cells for assessing tumor cell viability, colony formation, cell cycle distribution, apoptosis, xenograft formation, and growth in nude mice. Levels of β-catenin expression were markedly decreased in BE(2)C cells. Downregulation of β-catenin was concomitantly accompanied by reductions in colony formation and invasion capacity and by growth inhibition of BE(2)C cells in vitro. The mechanism appears to be a G0/G1 phase arrest and induction of apoptosis. In vivo, both tumor volume and weight of β-catenin knockdown cells were obviously reduced compared to the control and parental cells.
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β-Catenin knockdown could effectively control growth of neuroblastoma cells in vitro and in nude mice, suggesting that targeting β-catenin may be useful in clinical control of neuroblastoma. Final Decision: yes