Fig. 2: Fadraciclib downregulates MCL-1, resulting in rapid induction of apoptosis in lines treated with 1 µM of fadraciclib for 4 and 24 h. SH-PTP2 was used as an internal AML cell lines. | Cell Death Discovery

Fig. 2: Fadraciclib downregulates MCL-1, resulting in rapid induction of apoptosis in lines treated with 1 µM of fadraciclib for 4 and 24 h. SH-PTP2 was used as an internal AML cell lines.

From: Interrogation of novel CDK2/9 inhibitor fadraciclib (CYC065) as a potential therapeutic approach for AML

Fig. 2: Fadraciclib downregulates MCL-1, resulting in rapid induction of apoptosis in lines treated with 1 µM of fadraciclib for 4 and 24 h. SH-PTP2 was used as an internal AML cell lines.

A Representative Western blot of OCI-AML3, MOLM-13, and MV4-11 cell protein loading control. B Densitometric analysis of serine 807/serine 811 (S807/S811) phosphorylated and total Rb. C Densitometric analysis of serine 2 (S2) phosphorylated RNAPII and total RNAPII. D Densitometric analysis of MCL-1. E Densitometric analysis of cleaved poly (ADP-ribose) polymerase-1 (PARP1). F Heatmap demonstrating fold changes relative to NDC of gene expression of OCI-AML3, MOLM-13, and MV4-11 cell lines treated with 0.75, 0.5, and 1 µM of fadraciclib, respectively, for 4 and 24 h. G Fold changes of CDK9, MCL1, PPP1R10, and E2F1 gene expression as compared with NDC. n = 3. Graphs depict mean ± SD (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001). Data were compared using the Student’s t-test.

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