p53β expression in the MKN45 gastric cancer cell line responds to 5-fluorouracil growth inhibition treatment
نویسندگان
چکیده
This study aims to explore the role of the p53β isoform in fluorouracil-induced growth inhibition of MKN45 gastric cancer cells. A Cell Counting Kit 8 (CCK8) assay was used to measure inhibition rates in gastric cancer cell cultures (lines MKN45 and SGC7901) treated with different concentrations of 5-fluorouracil (5-FU). The abundance of p53β and p53 mRNA was measured using the nested reverse transcription polymerase chain reaction (nRT-PCR) method; protein abundance of p53β and p53 was quantified using western blots. In MKN45 cells, the growth inhibition differed significantly between groups treated with different 5-FU doses (F = 31.682, P < 0.01); this phenomenon was not observed for SGC7901 cells (F = 0.014, P > 0.05). In addition, growth inhibition differed significantly between groups measured at different time-points for MKN45 cells treated with 25 μg/mL 5-FU (F = 225.304, P < 0.01), but not for SGC7901 cells (F = 0.043, P > 0.05). The mRNA expression for p53 and p53β differed significantly between groups treated with different 5-FU doses (Fp53 = 187.992, Fp53β = 23.020, P < 0.01) in MKN but not in SGC7901 cells (Fp53 = 1.912, P = 0.206; Fp53β = 1.626, P = 0.259). Protein expression for p53 and p53β differed significantly between groups treated with different 5-FU doses (Fp53 = 80.646, Fp53β = 213.419, P < 0.01) in MKN but not in SGC7901 cells (Fp53 = 0.055, P = 0.982; Fp53β = 1.613, P = 0.261). p53β is an important oncotarget of 5-FU in the growth inhibition of MKN45 gastric cancer cells.
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Role of p53β in the inhibition of proliferation of gastric cancer cells expressing wild-type or mutated p53.
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