miR-126 Regulates Distinct Self-Renewal Outcomes in Normal and Malignant Hematopoietic Stem Cells

(Cancer Cell 29, 214–228; February 8, 2016) During figure preparation for this article, the authors inadvertently duplicated representative flow plots within Figure 3A (gated plot on left and lower right plot) and within Figures 4A and 4B (CTRL, AML17 and 126OE, AML17). The authors regret this error and apologize for any confusion that it may have caused. These errors have now been corrected in the figures here and in the article online.Figure 3Enforced Expression and Knockdown of miR-126 Alters the Proliferation and Differentiation Status of Primitive 8227 AML Cells (original)View Large Image Figure ViewerDownload Hi-res image Download (PPT)Figure 4Enforced Expression of miR-126 Expands Primary AML LSC (corrected)View Large Image Figure ViewerDownload Hi-res image Download (PPT)Figure 4Enforced Expression of miR-126 Expands Primary AML LSC (original)View Large Image Figure ViewerDownload Hi-res image Download (PPT) miR-126 Regulates Distinct Self-Renewal Outcomes in Normal and Malignant Hematopoietic Stem CellsLechman et al.Cancer CellJanuary 28, 2016In BriefLechman et al. show that miR-126 targets the PI3K/AKT/MTOR signaling pathway to preserve quiescence, increase self-renewal, and promote chemotherapy resistance of acute myeloid leukemia stem cells (LSC). Reducing the miR-126 level impairs LSC maintenance in contrast to expanding normal hematopoietic stem cells.