CREB knockdown inhibits growth and induces apoptosis in human pre-B acute lymphoblastic leukemia cells through inhibition of prosurvival signals
| Autor: | Ahmad Kazemi, Fatemeh Alikarami, Rima Manafi Shabestari, Majid Safa, Mehdi Banan |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Cell Survival p300-CBP coactivator family Apoptosis Pre-B Acute Lymphoblastic Leukemia CREB 03 medical and health sciences 0302 clinical medicine Precursor B-Cell Lymphoblastic Leukemia-Lymphoma hemic and lymphatic diseases Survivin Humans Cyclic AMP Response Element-Binding Protein Cell Proliferation Pharmacology Gene knockdown biology Chemistry HEK 293 cells General Medicine XIAP HEK293 Cells 030104 developmental biology Gene Knockdown Techniques 030220 oncology & carcinogenesis Cancer research biology.protein Signal transduction Signal Transduction |
| Zdroj: | Biomedicine & Pharmacotherapy. 87:274-279 |
| ISSN: | 0753-3322 |
| DOI: | 10.1016/j.biopha.2016.12.070 |
| Popis: | A majority of acute lymphoblastic leukemia patients overexpress CREB in the bone marrow. However, the functional significance of this up-regulation and the detailed molecular mechanism behind the regulatory effect of CREB on the growth of B-cell precursor acute lymphoblastic leukemia (BCP-ALL) cells has not been elucidated. We demonstrated here that CREB knockdown induced apoptosis and impaired growth of BCP-ALL NALM-6 cells which was associated with caspase activation. The gene expression levels of prosurvival signals Bcl-2, Mcl-1, Bcl-xL, survivin and XIAP were down-regulated upon CREB suppression. These findings indicate a critical role for CREB in proliferation, survival, and apoptosis of BCP-ALL cells. The data also suggest that CREB could possibly serve as potential therapeutic target in BCP-ALL. |
| Databáze: | OpenAIRE |
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