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. 2009 Sep 14;101(1):129–136. doi: 10.1111/j.1349-7006.2009.01367.x

Figure 2.

Figure 2

 Knockdown of prolyl‐4‐hydroxylase domain 2 (PHD2) results in increased resistance towards treatment with etoposide but not carboplatin. HeLa T‐Rex and 2.1.1‐16 cells were incubated in the presence or absence of 10 μg/mL tetracycline (Tet) for 48 h. Subsequently, cells were seeded in 96‐well plates and treated with the indicated concentrations of etoposide (A) or carboplatin (B) for 48 h. Etoposide and carboplatin‐induced cytotoxicity was analyzed by MTT assays. (n = 3 ± SD) *P < 0.05; **P < 0.01. (C) HeLa T‐Rex and 2.1.1‐16 cells were incubated in the presence or absence of 10 μg/mL Tet for 48 h. Subsequently, cells were seeded in 96‐well plates and treated with the indicated concentrations of etoposide for 48 h. Cell viability was analyzed using the MultiTox‐Fluor Multiplex Cytotoxicity Assay. (n = 3 ± SD) **P < 0.01. (D) Tet‐inducible PHD2 knockdown 2.1.1‐16 cells were incubated in the presence or absence of 10 μg/mL Tet for 48 h. Subsequently, cells were seeded in 96‐well plates and treated with 60 μm etoposide for 48 h as indicated. Cells were lysed and levels of activated caspase 3 and 7 as well as protein concentrations were determined. (n = 3 ± SEM) *P < 0.05. RLU, relative light units.