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. 2018 Feb 8;9(18):14539–14551. doi: 10.18632/oncotarget.24465

Figure 6. DNA methytransferase I and DNA topoisomerase II are mediators of miR-125b silencing in NPM-ALK-positive ALCL cells.

Figure 6

(A and B) Quantitative real-time PCR (qRT-PCR) analysis of miR-125b expression in NPM-ALK(+) ALCL KARPAS-299 cells treated for 48h or not (PBS) with 400 nM doxorubicin (A) or etoposide at a final concentration ranging from 100 to 300 nM (B). (C) Quantitative real-time PCR (qRT-PCR) analysis of miR-29a expression in NPM-ALK(+) ALCL KARPAS-299 cells treated for 48h or not (PBS) with doxorubicin or etoposide. SNORD44 served as an internal control and the level of hsa-miR-125b or miR-29a were expressed as 2–ΔΔCt relative to untreated cells. (D and E) ChIP experiments were performed using antibodies against DNMT1 (D) or histone H3 trimethylated on Lys-27 (H3K27me3) (E) on KARPAS-299 cells treated for 48h or not (PBS) with doxorubicin. Results are expressed as a ChIP enrichment relative to the untreated condition (PBS). (F) qRT-PCR analysis of the expression of pri-miR125b1 in KARPAS-299 cells treated or not (PBS) with doxorubicin. Actin mRNA was used as the internal control and the relative ratio of pri-miR125b1 expression was expressed as 2–ΔΔCt relative to untreated cells. (Data represent means ± SEM (bars) from 3 independent experiments. *P < 0.05, **P < 0.001, ***P < 0.0001; unpaired 2-tailed Student's t test.