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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, Blotting, Western, Cell Proliferation, Gene Expression Regulation, Neoplastic, Humans, Hypoglycemic Agents, Inflammation, Mice, Mice, Nude, NF-kappa B, Pioglitazone, Retinal Neoplasms, Retinoblastoma, Signal Transduction, Thiazolidinediones, Tumor Cells, Cultured, Xenograft Model Antitumor Assays.
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Does pioglitazone inhibit growth of human retinoblastoma cells via regulation of NF-κB inflammation signals? Context: We aimed to study the antitumor effects of the PPARγ agonist pioglitazone on human retinoblastoma. The effects of pioglitazone on cell proliferation and apoptosis of the human retinoblastoma Y79 cells were investigated by MTT assay and Hoechst 33258 staining assay. The apoptosis related protein levels were detected by western blot. Inflammationary factors analysis was evaluated by western blot and ELISA. The effect of pioglitazone on nuclear factor-kappa B (NF-κB)-dependent reporter gene transcription induced by LPS was analyzed by NF-κB-luciferase assay. Then human retinoblastoma Y79 cells were subcutaneously transplanted in BALB/c nude mice and the animals were treated with pioglitazone to verify its antitumor effect in vivo. Our data revealed that pioglitazone suppressed the viability of Y79 cells dose- and time-dependently and induced apoptosis in Y79 cells in vitro. Molecular biology analysis found that pioglitazone could affect the apoptosis and inflammation related signal via modulating the activity of NF-κB signal. Also we found that pioglitazone could markedly reduce the growth of Y79 cells transplanted into the mice without causing significant side effects.
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Our results suggested that pioglitazone demonstrated antitumor activity against the human retinoblastoma Y79 cells by inhibiting cell growth, inducing apoptosis and modulating NF-κB pathway, and thus delayed tumor growth in vivo. Final Decision: yes