AI Article Synopsis
- Acute myeloid leukemia (AML) develops from complex biological processes that are not fully understood, but recent epigenetic research shows potential for new therapies.
- Researchers studied the impact of the histone deacetylase (HDAC)2 on miRNA networks in U937 leukemic cells to further understand AML.
- The analysis revealed that miR-96-5p and miR-92a-3p may influence the disease's development by targeting specific genes, highlighting the value of alternative treatment approaches.
Article Abstract
Acute myeloid leukemia (AML) arises from a complex sequence of biological and finely orchestrated events that are still poorly understood. Increasingly, epigenetic studies are providing exciting findings that may be exploited in promising and personalized cutting-edge therapies. A more appropriate and broader screening of possible players in cancer could identify a master molecular mechanism in AML. Here, we build on our previously published study by evaluating a histone deacetylase (HDAC)2-mediated miRNA regulatory network in U937 leukemic cells. Following a comparative miRNA profiling analysis in genetically and enzymatically HDAC2-downregulated AML cells, we identified miR-96-5p and miR-92a-3p as potential regulators in AML etiopathology by targeting defined genes. Our findings support the potentially beneficial role of alternative physiopathological interventions.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6790563 | PMC |
| http://dx.doi.org/10.1002/1873-3468.13521 | DOI Listing |
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