[Effect of PDK1 on Notch1-Induced Mouse T-cell Acute Lymphoblastic Leukemia]
| Autor: | Le, Wang, Tian-Yuan, Hu, Xing, Chen, Cong, Li, Hui-Dong, Guo, Ya-Jing, Chu, Xiao-Min, Wang, Wei-Li, Wang, Tao, Cheng, Wei-Ping, Yuan |
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| Rok vydání: | 2016 |
| Předmět: |
Mice
Knockout Gene Expression Regulation Leukemic Cell Cycle NF-kappa B Pyruvate Dehydrogenase Acetyl-Transferring Kinase Apoptosis Protein Serine-Threonine Kinases Precursor T-Cell Lymphoblastic Leukemia-Lymphoma Real-Time Polymerase Chain Reaction Proto-Oncogene Proteins c-myc Disease Models Animal Mice Animals Receptor Notch1 Tumor Suppressor Protein p53 |
| Zdroj: | Zhongguo shi yan xue ye xue za zhi. 24(3) |
| ISSN: | 1009-2137 |
| Popis: | To explore the role of PDK1 in T-ALL development through establishing the Notch1-induced T-ALL mouse model by using Mx1-cre; LoxP system to knock-out PDK1.Cell cycle and apoptosis of leukemic cells were detected by flow cytometry, and relative expression of tumor-related genes and transcription factors of leukemic cells were determined by quantitative real-time PCR.Notch1-induced T-ALL mouse model with inducible knock-out of PDK1 was established successfully. Compared to T-ALL control mouse model, PDK1 knock-out mice showed a significant longer survival time (P0.01). There was no difference of cell cycle between control and PDK1 knock-out mice, and the apoptosis rate of leukemic cells in PDK1 knock-out mice was higher than that of control mice (P0.001). PDK1 knock-out resulted in decreased expression of tumor-related genes and transcription factors, such as c-Myc and NF-κB (P0.01), and increased expression level of P53 (P0.01).PDK1 knock-out can inhibit the development of T-ALL, and its mechanism may be the leukemia progression inhibited by regulating the apoptosis and expression of multiple related genes and transcription factors. |
| Databáze: | OpenAIRE |
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