Figure 2.
Inhibition of SOX9 in IGH-BCL2+ DLBCL cells impairs cell survival and proliferation. Immunoblot (A) and CFSE proliferation (B) assays of SOX9− Karpas-422 and DB cells. (C) Hemocytometer counts of the number of SOX9− Karpas-422 and DB cells. (D) SOX9− Karpas-422 and DB cells were exposed to BrdU for 4 hours before flow cytometry analysis. Quantitation of the percentage distribution of cell cycle phases was determined by gating of live cells in the G1 (light gray bar), S (dark gray bar), or G2 (white bar) phases. (E) Immunoblot assay of expression of Bcl-xL, Mcl-1, Bcl-2, Bad, and Bax. β-Actin was included as the control for equal loading. (C-D) Data represent the mean ± SD of technical triplicates. ****P < .005. CFSE, carboxyfluorescein diacetate succinimidyl ester.

Inhibition of SOX9 in IGH-BCL2+ DLBCL cells impairs cell survival and proliferation. Immunoblot (A) and CFSE proliferation (B) assays of SOX9 Karpas-422 and DB cells. (C) Hemocytometer counts of the number of SOX9 Karpas-422 and DB cells. (D) SOX9 Karpas-422 and DB cells were exposed to BrdU for 4 hours before flow cytometry analysis. Quantitation of the percentage distribution of cell cycle phases was determined by gating of live cells in the G1 (light gray bar), S (dark gray bar), or G2 (white bar) phases. (E) Immunoblot assay of expression of Bcl-xL, Mcl-1, Bcl-2, Bad, and Bax. β-Actin was included as the control for equal loading. (C-D) Data represent the mean ± SD of technical triplicates. ****P < .005. CFSE, carboxyfluorescein diacetate succinimidyl ester.

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