Musashi2 modulates K562 leukemic cell proliferation and apoptosis involving the MAPK pathway
Copyright policy )Musashi2 modulates K562 leukemic cell proliferation and apoptosis involving the MAPK pathway
The RNA-binding protein Musashi2 (Msi2) has been identified as a master regulator within a variety of stem cell populations via the regulation of translational gene expression. A recent study has suggested that Msi2 is strongly expressed in leukemic cells of acute myeloid leukemia patients, and elevated Msi2 is associated with poor prognosis. However, the potential role of Msi2 in leukemogenesis is still not well understood. Here, we investigated the effect of Msi2 knockdown on the biological properties of leukemic cells. High expression of Msi2 was found in K562 and KG-1a leukemic cell lines, and low expression was observed in the U937 cell line. We transduced K562 cells with two independent adenoviral shRNA vectors targeting Msi2 and confirmed knockdown of Msi2 at the mRNA and protein levels. Msi2 silencing inhibited cell growth and caused cell cycle arrest by increasing the expression of p21 and decreasing the expression of cyclin D1 and cdk2. In addition, knockdown of Msi2 promoted cellular apoptosis via the upregulation of Bax and downregulation of Bcl-2 expression. Furthermore, Msi2 knockdown resulted in the inactivation of the ERK/MAPK and p38/MAPK pathways, but no remarkable change in p-AKT was observed. These data provide evidence that Msi2 plays an important role in leukemogenesis involving the MAPK signaling pathway, which indicates that Msi2 may be a novel target for leukemia treatment.
- Chongqing Medical University China (People's Republic of)
MAP Kinase Signaling System, RNA-Binding Proteins, Apoptosis, HL-60 Cells, U937 Cells, HEK293 Cells, Humans, Mitogen-Activated Protein Kinases, K562 Cells, Cells, Cultured, Cell Proliferation
MAP Kinase Signaling System, RNA-Binding Proteins, Apoptosis, HL-60 Cells, U937 Cells, HEK293 Cells, Humans, Mitogen-Activated Protein Kinases, K562 Cells, Cells, Cultured, Cell Proliferation
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