Project description:Myeloid progenitor cells have generally been considered the exclusive source of myeloid cells under steady-state conditions. Here, we show that NK cells contributed to a myeloid cell lineage pool in naïve and tumor-bearing mice. By using fate tracing of NKp46+ cells, we found evidence that myeloid cell populations could be derived from NK-committed NKp46+ cells. Notably, among mature CD11b+CD27+ NK cells, c-Kit+CD24+ NK cells were capable of differentiating into a range of myeloid lineages in vitro and reprogrammed into neutrophils and monocytes in vivo. In addition to the potential for lineage conversion, c-Kit+CD24+ NK cells retained NK cell phenotypes and effector functions. Mechanistically, GATA-2 was essential for the conversion of the c-Kit+CD24+ NK cells into myeloid cells. Therefore, we discovered that GATA-2-mediated conversion of c-Kit+CD24+ NK cells contributes to myeloid cell development and identified a novel pathway for myeloid lineage commitment in physiological conditions.
Project description:Here we interrogate CD32A protein interactions in the cytoplasm and membrane fractions isolated from the human AML cell lines K562 wild-type and knockout for CD32A. Cells were fractionated prior to incubation with CD32A antibody and subsequent samples isolated using protein agarose beads.
Project description:Expression profiling of CD24+ and CD24- population cells from myeloma cell lines. Results provide insight into the role of CD24+ cells in myeloma development. Keywords: multiple myeloma, cancer stem cell, CD24
Project description:To understand whether CD24, a potential marker for ovarian cancer stem cells,-dependent microRNA expression affects ovarian cancer stemness, microRNA expression was compared between CD24-negative and CD24-positive ovarian cancer cells.
Project description:To understand the role of p53 in regulating stem cell population (CD24-CD44+) and stemness-associated miRNAs, we first compared miRNA expression profiles between human mammary epithelical cells knocked-down p53 and control cells. We then cross-referenced p53-regulated miRNAs with stemness-associated miRNAs analyzed from expression profiling of sorted CD24-CD44+ and non-CD24-CD44+ cell populations. Further biological experiments were performed with the miRNAs that are altered in CD24-CD44+ stem cell populations and also regulated by p53.
Project description:Being involved in adhesion, migration, and invasion, the highly glycosylated signal transducer CD24 (cluster of differentiation 24) has been implicated to play an essential role during carcinogenesis. Previously, the molecular and (epi)genetic regulation of CD24 has been characterized in testicular germ cell tumors (GCT). Here, CD24 was exclusively found in embryonal carcinoma (EC), which represents the stem cell like population of GCT (see project PXD025110). For a better understanding of the molecular function of CD24, this study aimed at the identification of the direct interaction partners of CD24 not only in GCTs, but also in other urologic malignancies, such as urothelial- (UC), prostate- (PC), and renal cell carcinoma (RCC). For this purpose, co-immunoprecipitations of CD24 were performed in GCT, UC, PC, and RCC cell lines, while CD24-deficient EC cells as well as IgG2a controls were included for high validity. Extracted proteome was measured by liquid-chromatography coupled with mass spectrometry (LS-MS).