Journal: Cellular Oncology

Article Title: NR2F2/AGAP2 axis: regulating lipid synthesis to drive AML progression via AMPKα/ACC pathway

doi: 10.1007/s13402-026-01184-8

Figure Lengend Snippet: AGAP2 inhibited cell differentiation via targeting AMPK/ACC pathway. KG-1 and HL-60 cells were subjected to lentiviral transduction, and then were treated with 30 µM GSK621 for 48 h to activate AMPK. ( A ) Giemsa staining was used to assess cell morphology and differentiation, ×400 magnification. B , C . Analysis of differentiation marker CD11b expression by flow cytometry under AGAP2 overexpression. ( B ) Representative flow cytometry histograms; ( C ) Quantitative analysis of CD11b-positive cells. D , E . CD11b expression was analyzed by flow cytometry in cells co-transduced with a non-targeting control shRNA (NC), AGAP2-targeting shRNA (shAGAP2), or both AGAP2- and AMPKα1-targeting shRNAs (shAGAP2+ shAMPKα1). N = 3. The data were present as mean ± SD. N represents biological replicates. Error bars denote SD. * comparison of the EV group and AGAP2 group or comparison of the NC group and shAGAP2 group; * p < 0.05; ** p < 0.01; *** p < 0.005. # comparison of the AGAP2 group and AGAP2 + GSK621 group, or comparison of the shAGAP2 group and shAGAP2+shAMPKα1 group; # p < 0.05; ## p < 0.05; ### p < 0.005

Article Snippet: Subsequently, 100 μL of staining buffer was added and mixed thoroughly, followed by the addition of 5 μL of CD11b antibody (#E-AB-F1081D, Elabscience, China).

Techniques: Cell Differentiation, Transduction, Staining, Marker, Expressing, Flow Cytometry, Over Expression, Control, shRNA, Comparison