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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, Carcinoma, Cell Proliferation, Gene Expression Regulation, Neoplastic, Genetic Therapy, Humans, Lentivirus, Male, Mice, Mice, Nude, MicroRNAs, Stomach Neoplasms, Tumor Cells, Cultured, Up-Regulation.
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Does lentiviral vector-mediated upregulation of let-7a inhibit gastric carcinoma cell growth in vitro and in vivo? Context: Let-7a, a molecule that is reduced in various cancers, has been associated with cell growth and proliferation. Upregulation of let-7a may inhibit tumor cell growth. To verify this hypothesis, let-7a gene overexpression was studied in gastric cancer cells in vitro and in vivo. A lentiviral system harboring both enhanced green fluorescent protein reporter gene and the let-7a short hairpin RNA expression cassette was firstly constructed. Then the stable let-7a gene overexpression SGC-7901 cells were established and real-time RT-PCR analysis was used to evaluate the expression of the let-7a gene. Their growth-inhibiting, cell cycle arrest characteristics were identified. In SGC-7901/let-7a cells, let-7a expression was significantly increased. Their proliferation was obviously retarded and the cell cycle changed with increased G0/G1 arrest and decreased S phase. In animal experiments, SGC-7901/let-7a cell xenografts demonstrated growth suppression compared to parental or control gastric cancer cell xenografts.
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The results demonstrated that lentiviral vector was capable of upregulating let-7a, resulting in impressive anticancer effects. It offers a powerful new strategy for the development of novel therapeutic interventions to treat human gastric carcinomas. Final Decision: yes