AI Article Synopsis
- The study aimed to explore how NF-κB inhibitors affect the occurrence and progression of Acute Myeloid Leukemia (AML).
- Researchers collected bone marrow samples from 8 AML patients and 8 healthy individuals to analyze NF-κB signaling pathway genes using a PCR array, and they also created an AML mouse model to test the NF-κB inhibitor’s effects.
- Results showed that the NF-κB pathway is activated in AML, with certain genes promoting inflammation and others leading to cell death; administering the inhibitor helped normal hematopoietic stem cells to enter the cell cycle, indicating potential for AML treatment.
Article Abstract
Objective: To investigate the role of NF-κB inhibitor in occurence and development of AML.
Methods: AML and normal bone marrow samples were collected from 8 AML patients and 8 normal persons. The expression of NF-κB signaling pathway genes was detected by NF-κB PCR array. Then, AML mouse model was constructed to test the role of NF-κB inhibitor in AML.
Results: The NF-κB signal pathway was activated in AML patients. The up-regulated genes, EDARADD, TNFSF14, could activate the NF-κB signal pathway, IL6 could regulate the inflammatory signal. The down-regulated genes, TNFRSF 10B, TNFRSF1A, could lead to cell apoptosis. the AML mouse model was constructed successfully. Then administration of NF-κB inhibitor reduced the inhibition of leukemia niche to the normal hematopoietic stem cells (HSCs), promoted the HSC to enter into cell cycle.
Conclusion: The NF-κB signal pathway is activated in AML cells. AML mouse model is constructed successfully. NF-κB inhibitor has a potential to treat AML and promotes the HSC to enrter into cell cycle.
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| http://dx.doi.org/10.7534/j.issn.1009-2137.2016.06.002 | DOI Listing |
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