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

Figure 3.

Figure 3

 Knockdown of prolyl‐4‐hydroxylase domain 2 (PHD2) results in increased resistance towards treatment with vinblastine. (A) 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 vinblastine for 48 h. Vinblastine‐induced cytotoxicity was analyzed by MTT assays. (n = 3 ± SD) **P < 0.01. (B,C) 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 (B) or 300 μm carboplatin (C) in the absence or presence of 10 μm verapamil for 48 h. Etoposide‐induced cytotoxicity was analyzed by MTT assays. (n = 3 ± SEM) *P < 0.05. (D,E) 2.1.1‐16 cells were incubated in the presence or absence of 10 μg/mL Tet. Subsequently, MDR1 efflux activity (D) and MDR1 RNA expression (E) were analyzed. (n = 3 ± SD) *P < 0.05.