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. Author manuscript; available in PMC: 2014 Jun 10.
Published in final edited form as: Cancer Cell. 2013 Jun 10;23(6):826–838. doi: 10.1016/j.ccr.2013.05.002

Figure 4. HRK induction in DLBCL cell lines following SYK or PI3K inhibition.

Figure 4

(A) HRK transcript abundance in DLBCL cell lines following R406 treatment (24 hr) was determined by qRT-PCR. (B) HRK expression in SYK-depleted DLBCL cell lines was assessed by qRT-PCR. (C) HRK expression in the indicated cell lines following treatment with R406, LY294002, or vehicle for 24 hr assessed by qRT-PCR. (D) HRK transcript abundance in DLBCL lines transduced with mAKT or pMIG, FACS-sorted, then treated with R406 or vehicle for 24 hr was analyzed by qRT-PCR. (E) DHL4 cells stably transduced with the indicated HRK siRNA or negative control siRNA (NC) were treated with R406 or vehicle for 24 hr and analyzed for HRK transcript abundance by qRT-PCR. (F) Apoptosis of DHL4 cells transduced with HRK siRNA or negative control siRNA (NC) and treated with vehicle or R406 for 72 hr was assessed by Annexin V/PI staining. (G and H) Viable DLBCL tumor cells isolated from cryopreserved primary patient samples were analyzed for cell surface Ig expression (G) or for HRK and BCL2A1 transcript abundance after treatment with R406 or vehicle for 24 hr by qRT-PCR (H). p-values for vehicle vs. R406 (A and H), vehicle vs. R406 or LY29004 (C), NC vs. shSYK (B) and pMIG +R406 vs. mAKT +R406 (D) were determined with a one-sided Welch t-test. ***, p≤0.0001; **, p≤0.001; *, p≤0.01. Error bars represent the SD of 3 independent assays in a representative experiment. See also Figure S4.