A1 induces G0/G1 phase arrest with NOXA induction-mediated cyclin D1 reduction in Bcl-xL expressing cells. (A) Growth inhibition by DHA, VEN, DHA + VEN, and A1 in KCL22 and K562 cells treated for 72 hours. (B) Apoptosis induction in KCL22 and K562 cells treated with 0.8 μM DHA, VEN, DHA + VEN, and A1 for 24 hours. Apoptotic cells were quantified using FACS after staining with annexin V/PI. (C) Cell cycle distribution of KCL22 and K562 cells treated with 0.8 μM DHA, VEN, DHA + VEN, and A1 for 24 hours and assessed by FACS after PI staining. (D) Protein regulation of KCL22 and K562 cells treated with A1 at the indicated concentrations for 24 hours. The downward column figures are image density analyses of 3 independent experiments. (E) K562 cells transfected with Bcl-xL (BCL2L1)-small interfering RNA (siRNA) for 24 hours, followed by treatment with 0.8 μM A1 for 24 hours. (F) K562 cells treated with 0.8 μM A1, 0.8 μM A1155463 alone, and their combination for 24 hours. Apoptotic cells were quantified using FACS after staining with annexin V/PI. The relative protein levels were determined by western blotting. (G) Growth inhibition of KV2 (transfected with an empty vector) and KB8 (transfected with Bcl-xL expressing vector) cells treated with A1 for 72 hours. (H) Apoptosis induction of KV2 and KB8 cells treated with A1 at the indicated concentrations for 24 hours. Apoptotic cells were quantified using FACS after staining with annexin V/PI. (I) Cell cycle distribution of KV2 and KB8 cells treated with A1 for 24 hours and assessed by FACS after PI staining. (J) The relative protein levels of KV2 and KB8 cells treated with A1 for 24 hours. The right column figures are image density analyses of 3 independent experiments. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001 when compared with the control group. ##P < .01; ###P < .001 2-group analysis. BimEL, Bim extralong; BimL, Bim long; BimS, Bim short; Con, control; siCtrl, small interfering RNA control.

A1 induces G0/G1 phase arrest with NOXA induction-mediated cyclin D1 reduction in Bcl-xL expressing cells. (A) Growth inhibition by DHA, VEN, DHA + VEN, and A1 in KCL22 and K562 cells treated for 72 hours. (B) Apoptosis induction in KCL22 and K562 cells treated with 0.8 μM DHA, VEN, DHA + VEN, and A1 for 24 hours. Apoptotic cells were quantified using FACS after staining with annexin V/PI. (C) Cell cycle distribution of KCL22 and K562 cells treated with 0.8 μM DHA, VEN, DHA + VEN, and A1 for 24 hours and assessed by FACS after PI staining. (D) Protein regulation of KCL22 and K562 cells treated with A1 at the indicated concentrations for 24 hours. The downward column figures are image density analyses of 3 independent experiments. (E) K562 cells transfected with Bcl-xL (BCL2L1)-small interfering RNA (siRNA) for 24 hours, followed by treatment with 0.8 μM A1 for 24 hours. (F) K562 cells treated with 0.8 μM A1, 0.8 μM A1155463 alone, and their combination for 24 hours. Apoptotic cells were quantified using FACS after staining with annexin V/PI. The relative protein levels were determined by western blotting. (G) Growth inhibition of KV2 (transfected with an empty vector) and KB8 (transfected with Bcl-xL expressing vector) cells treated with A1 for 72 hours. (H) Apoptosis induction of KV2 and KB8 cells treated with A1 at the indicated concentrations for 24 hours. Apoptotic cells were quantified using FACS after staining with annexin V/PI. (I) Cell cycle distribution of KV2 and KB8 cells treated with A1 for 24 hours and assessed by FACS after PI staining. (J) The relative protein levels of KV2 and KB8 cells treated with A1 for 24 hours. The right column figures are image density analyses of 3 independent experiments. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001 when compared with the control group. ##P < .01; ###P < .001 2-group analysis. BimEL, Bim extralong; BimL, Bim long; BimS, Bim short; Con, control; siCtrl, small interfering RNA control.

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