Figure 2.
Patients with AML with high SMARCD1 levels harbor transcriptomic signatures of leukemic stem cells and show poor prognosis. (A-E) SMARCD1 regulates myeloid differentiation in patient-derived CD34+ HSPCs. (A) Log2 fold change of SMARCD1 expression calculated with respect to shcontrol cells using RT-PCR and (B) Western blot showing reduction in SMARCD1 levels on lentiviral transduction and after 96 hours of puromycin selection. ACTB mRNA was used for normalizing SMARCD1 expression in RT-PCR, and ACTB was used as the protein loading control. (C-D) Contour plots showing percentage of double-positive CD11b and CD14 cells and MFI plots of shcontrol and shSMARCD1-transduced CD34+ HSPCs. (E-F) Bright field images of shcontrol and shSMARCD1 cells in culture (E) and May Grünwald Giemsa (F) staining showing nucleo-cytoplasmic morphologic features. Error bars indicate means ± standard deviation. *P = .05; **P = .005: 2-tailed Student t test. (F-K) Transcriptomic signatures of AML patients with high and low SMARCD1 gene expression. Patients with AML from the TCGA cohort were stratified in the top and bottom 10th percentile as SMARCD1high and SMARCD1low groups. (F) Principal component analysis plots of SMARCD1high and SMARCD1low groups depicting clear segregation of the samples from TCGA. (G) Gene set enrichment analysis of transcriptomic signatures in SMARCD1high and SMARCD1low groups from AML TCGA cohorts. Normalized enrichment score (NES). (H) Z-score–normalized heat map representation of bona fide differentiation- and stemness-related genes in SMARCD1high and SMARCD1low groups from AML TCGA cohort. (I) Relative log2 fold change of indicated genes in CD34+ AML cells compared with that in the CD34− population. Error bars indicate means ± standard deviation; 2-tailed Student t test. (K) Correlation analysis showing positive correlation of AML patients in TCGA cohort with different levels of blast percentage (i) and negative correlation of SMARCD1 expression with percentage of monocytes present in peripheral blood of patients with AML in the BEAT AML cohort (ii).

Patients with AML with high SMARCD1 levels harbor transcriptomic signatures of leukemic stem cells and show poor prognosis. (A-E) SMARCD1 regulates myeloid differentiation in patient-derived CD34+ HSPCs. (A) Log2 fold change of SMARCD1 expression calculated with respect to shcontrol cells using RT-PCR and (B) Western blot showing reduction in SMARCD1 levels on lentiviral transduction and after 96 hours of puromycin selection. ACTB mRNA was used for normalizing SMARCD1 expression in RT-PCR, and ACTB was used as the protein loading control. (C-D) Contour plots showing percentage of double-positive CD11b and CD14 cells and MFI plots of shcontrol and shSMARCD1-transduced CD34+ HSPCs. (E-F) Bright field images of shcontrol and shSMARCD1 cells in culture (E) and May Grünwald Giemsa (F) staining showing nucleo-cytoplasmic morphologic features. Error bars indicate means ± standard deviation. *P = .05; **P = .005: 2-tailed Student t test. (F-K) Transcriptomic signatures of AML patients with high and low SMARCD1 gene expression. Patients with AML from the TCGA cohort were stratified in the top and bottom 10th percentile as SMARCD1high and SMARCD1low groups. (F) Principal component analysis plots of SMARCD1high and SMARCD1low groups depicting clear segregation of the samples from TCGA. (G) Gene set enrichment analysis of transcriptomic signatures in SMARCD1high and SMARCD1low groups from AML TCGA cohorts. Normalized enrichment score (NES). (H) Z-score–normalized heat map representation of bona fide differentiation- and stemness-related genes in SMARCD1high and SMARCD1low groups from AML TCGA cohort. (I) Relative log2 fold change of indicated genes in CD34+ AML cells compared with that in the CD34− population. Error bars indicate means ± standard deviation; 2-tailed Student t test. (K) Correlation analysis showing positive correlation of AML patients in TCGA cohort with different levels of blast percentage (i) and negative correlation of SMARCD1 expression with percentage of monocytes present in peripheral blood of patients with AML in the BEAT AML cohort (ii).

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