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. Author manuscript; available in PMC: 2015 Aug 26.
Published in final edited form as: Oncogene. 2014 Mar 24;34(9):1073–1082. doi: 10.1038/onc.2014.61

Figure 5.

Figure 5

BCL6 inhibition decreases the viability of breast cancer cells. (A) MDA-MB-468 breast cancer cells were treated with RI-BPI or control peptide for twelve hours and then expression of BCL6 target genes were analyzed by qRT-PCR. (B) Breast cancer cells were treated with the indicated doses of RI-BPI or control peptide (µM) for 48 hours after which viable cell number was determined. (C) MDA-MB-468 breast cancer cells were treated with 15 µM RI-BPI for 48 hours and then initiation of apoptosis was determined by immunoblot for PARP cleavage. HSP90 served as a loading control. (D) MDA-MB-468 cells were treated with vehicle or 15 µM RI-BPI for 48 hours after which apoptosis was determined by Annexin V/PI staining and flow cytometry. (E) MDA-MB-468 cells treated with control or BCL6-targeted siRNA were then treated with vehicle or RI-BPI for 48 hours and viable cell number was measured. (F) MDA-MB-468 cells were transfected with siRNA to BCL6 and/or Jak2. Relative cell viability was measured after 72 hours. (G) MDA-MB-468 cells treated with control or Jak2-targeted siRNA were treated with 10 µM RI-BPI for 48 hours and viable cell number was determined. (H) MDA-MB-468 cells transfected with siRNA to BCL6 were treated with the Jak2 inhibitor TG101348 (3 µM) for 48 hours and cell viability was measured. (I) MDA-MB-468 cells were treated with 10 µM RI-BPI (BPI) and the indicated doses of TG101348 for 48 hours and then cell viability was measured.