| First Author | Jia Q | Year | 2017 |
| Journal | Biochem Biophys Res Commun | Volume | 487 |
| Issue | 4 | Pages | 868-874 |
| PubMed ID | 28461114 | Mgi Jnum | J:253915 |
| Mgi Id | MGI:6101666 | Doi | 10.1016/j.bbrc.2017.04.144 |
| Citation | Jia Q, et al. (2017) miR-17-92 promotes leukemogenesis in chronic myeloid leukemia via targeting A20 and activation of NF-kappaB signaling. Biochem Biophys Res Commun 487(4):868-874 |
| abstractText | miR-17-92 cluster are overexpressed in hematological malignancies including chronic myeloid leukemia (CML). However, their roles and mechanisms that regulate BCR-ABL induced leukemogenesis remain unclear. In this study, we demonstrated that genomic depletion of miR-17-92 inhibited the BCR-ABL induced leukemogenesis by using a mouse model of transplantation of BCR-ABL transduced hematopoietic stem cells. Furthermore, we identified that miR-19b targeted A20 (TNFAIP3). A20 overexpression results in inactivation of NF-kappaB activity including decrease of phosphorylation of P65 and IkappaBalpha, leads to induce apoptosis and inhibit proliferation and cycle in CML CD34 (+) cells. Thus we proved that miR-17-92 is a critical contributor to CML leukemogenesis via targeting A20 and activation of NF-kappaB signaling. These findings indicate that miR-17-92 will be important resources for developing novel treatment strategies of CML and better understanding long-term disease control. |
