Figure 5.
TIM-3 signaling induces β-catenin accumulation in accordance with p120-catenin expression level in AML. (A) FACS analysis of the expression of TIM-3 on CD34+CD38– (middle; LSCs-enriched fraction) and CD34+CD38+ (right; main blasts–enriched fraction) AML cells from the CD45dimSSClow fraction. Representative FACS plots of 4 independent AML samples (AML#7, #8, #13, and #14) are shown. (B) RT-qPCR analysis of the expression of CTNND1 mRNA in LSCs compared with blasts from AML samples of 3 independent AML cases. Results were normalized to the mRNA expression of GAPDH. Data are presented as mean ± SEM, ∗∗P < .01 and ∗P < .05. (C) WB analysis of cell lysate from Gal-9–stimulated CD34+CD38– AML cells (LSCs) and CD34+CD38+ cells (blasts) (AML#14). Of note, LSCs with higher p120-catenin expression exhibited profound β-catenin accumulation.

TIM-3 signaling induces β-catenin accumulation in accordance with p120-catenin expression level in AML. (A) FACS analysis of the expression of TIM-3 on CD34+CD38 (middle; LSCs-enriched fraction) and CD34+CD38+ (right; main blasts–enriched fraction) AML cells from the CD45dimSSClow fraction. Representative FACS plots of 4 independent AML samples (AML#7, #8, #13, and #14) are shown. (B) RT-qPCR analysis of the expression of CTNND1 mRNA in LSCs compared with blasts from AML samples of 3 independent AML cases. Results were normalized to the mRNA expression of GAPDH. Data are presented as mean ± SEM, ∗∗P < .01 and ∗P < .05. (C) WB analysis of cell lysate from Gal-9–stimulated CD34+CD38 AML cells (LSCs) and CD34+CD38+ cells (blasts) (AML#14). Of note, LSCs with higher p120-catenin expression exhibited profound β-catenin accumulation.

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