Fig. 5: Depletion of CALCRL sensitizes AML cells to chemotherapy through induction of DNA damages. | Nature Communications

Fig. 5: Depletion of CALCRL sensitizes AML cells to chemotherapy through induction of DNA damages.

From: Adrenomedullin-CALCRL axis controls relapse-initiating drug tolerant acute myeloid leukemia cells

Fig. 5

a Four days after transduction, MOLM-14 or OCI-AML3 cells were treated with AraC or idarubicin for 48 h. Then cell viability was assessed by MTS assay and values were normalized to untreated condition (n = 3 independent experiments). Curve fit to calculate IC50 was determined by log (inhibitor) vs response (three parameters). b Graph shows the percentage of AnnV+ or 7-AAD+ cells. Four days after transduction, cells were treated with chemotherapeutic agents for 48 h before flow cytometry analysis (n = 4 independent experiments, unpaired t-test). c Colonies in methylcellulose were counted 1 week after transfection of primary AML samples with siCTR or siCAL+/- 5 nM AraC (n = 7 primary AML samples, paired t-est). d Detection of double strand breaks by alkaline comet assays in MOLM-14 cells untreated or treated 24 h with Ara-C (1 µM). Representative pictures of nuclei in the same experiment. e Quantification of alkaline comet tail moments for one representative experiment (135–413 nuclei were analyzed for each treatment, unpaired t-test) out of four. Data are mean ± s.e.m.

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