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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 Regulatory Proteins, Carcinogenesis, Disease Models, Animal, Gene Expression Regulation, Neoplastic, Gene Transfer Techniques, Genetic Therapy, Humans, Lung Neoplasms, Mice, Oncogene Protein p21(ras), Polyethyleneimine, Proto-Oncogene Proteins c-akt, RNA, Small Interfering, RNA-Binding Proteins.
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Does dual expression of shAkt1 and Pdcd4 suppress lung tumorigenesis in K-rasLA1 mice? Context: Lung cancer has the highest mortality rate among cancers and current therapies are not efficient. Therefore, novel therapeutic methods are urgently needed. Here, we examined the effectiveness of simultaneous Akt1 inhibition and Pdcd4 over-expression using a dual expression system in suppressing tumorigenesis in K-ras(LA1) mice (a lung cancer model). An shRNA targeting Akt1 (shAkt1) and cDNA of programmed cell death protein 4 (Pdcd4) were inserted into a dual expression vector (shAkt1+Pdcd4). A sorbitol diacrylate-polyethylenimine (SDA-PEI) carrier was used because of low toxicity and high transfection efficiency. Aerosolized SDA-PEI/shAkt1+Pdcd4 complex was delivered to the mice twice a week for 4 weeks using a nose-only exposure inhalation chamber. Simultaneous Akt1 inhibition and Pdcd4 over-expression synergistically induced potent antitumor effect. Analysis revealed significant reduction in lung tumor number.
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Dual expression of shAkt1 and Pdcd4 effectively suppresses lung tumorigenesis. Final Decision: yes