American Society of Hematology

Figure 2.

$Pharmacological inhibition of PRMT5 induces apoptosis and mitigates tumor growth. (A) Treatment of BPDCN (CAL-1) and AML (THP-1, MOLM-13, MV-4-11) cells with GSK3326595. Decrease in (B) PRMT5 and (C) MYC mRNA expression after 72 hours of treatment. (D) Reduction in SDMA levels upon GSK595 treatment. (E) A dose-dependent increase in apoptotic fraction after treatment. (F) Expression of anti (BCL-2) and proapoptotic (PUMA) genes in GSK595-treated CAL-1 cells, normalized to DMSO. (G) Schematic illustration of treatment regimen (created with BioRender.com) (H) Decrease in tumor volume in GSK595-treated mice compared with vehicle-treated. (I) Loss of SDMA expression in tumors harvested from treated mice. (J) Mice body weight upon treatment with vehicle or GSK595. Data are shown as mean ± standard error of the mean of 3 independent experiments. *P < .05; **P < .01; ***P < .001.$

Pharmacological inhibition of PRMT5 induces apoptosis and mitigates tumor growth. (A) Treatment of BPDCN (CAL-1) and AML (THP-1, MOLM-13, MV-4-11) cells with GSK3326595. Decrease in (B) PRMT5 and (C) MYC mRNA expression after 72 hours of treatment. (D) Reduction in SDMA levels upon GSK595 treatment. (E) A dose-dependent increase in apoptotic fraction after treatment. (F) Expression of anti (BCL-2) and proapoptotic (PUMA) genes in GSK595-treated CAL-1 cells, normalized to DMSO. (G) Schematic illustration of treatment regimen (created with BioRender.com) (H) Decrease in tumor volume in GSK595-treated mice compared with vehicle-treated. (I) Loss of SDMA expression in tumors harvested from treated mice. (J) Mice body weight upon treatment with vehicle or GSK595. Data are shown as mean ± standard error of the mean of 3 independent experiments. *P < .05; **P < .01; ***P < .001.

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