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. 2019 May 7;39(5):BSR20181374. doi: 10.1042/BSR20181374

Figure 1. Long-time gemcitabine treatment induces resistance and RRM2 increases in pancreatic cancer cells.

Figure 1

(A) MIA-PaCa2 cells and the derived long-time gemcitabine-treated subclone MIA-PaCa2-GEM were untreated (0 nM) or treated with gemcitabine in concentrations from 10 to 200 nM as indicated. The viability was measured by MTT assay 72 h after treatment. (B) cells were treated as described above followed by staining with Annexin V-FITC and PI 72 h later and evaluation by FACS-analysis. The percentage of FITC-positive cells is shown as ‘Apoptosis (%)’. (C and D) Total RNA and cytoplasmic proteins were extracted from MIA-PaCa2 and MIA-PaCa2-GEM cells, and the expression of RRM2 was analyzed by qRT-PCR (C) and Western blot (D). GAPDH and β-actin were used as controls. (E and F) MIA-PaCa2-GEM cells were treated with 100 nM specific or negative control siRNA in the presence or absence of gemcitabine (100 nM). Cells were harvested 72 h later. The expression of RRM2 was analyzed by qRT-PCR (E) and Western blot (F). (G) The viability was measured by MTT assay when treated by gemcitabine (100 nM) for 24, 48 and 72 h. Each experiment was performed three times; **P<0.01.