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. 2019 Apr 8;11(4):498. doi: 10.3390/cancers11040498

Figure 6.

Figure 6

HBE1-deficiency in radiation-resistant cells increases radiation sensitivity through increased reactive oxygen species (ROS) production and cell cycle arrest. After transfecting SW480-IR and HT-29-IR cells with control or HBE1 siRNA in the presence or absence of radiation (5 Gy) exposure, ROS production and the expression of HBE1 were measured by real-time PCR. (A) Intracellular ROS levels were analyzed by flow cytometry using CM-H2DCFDA for the indicated times, compared to those in the corresponding controls * p < 0.05, ** p < 0.01. (B) Bar graph showing that HBE1 depletion via HBE1 siRNA decreases the survival rate, as determined by a clonogenic assay, after 14 days. Cells were pre-treated with the antioxidant N-acetyl cysteine (NAC). * p < 0.05, ** p < 0.01 (C) Ionizing radiation (IR)-resistant cells were transfected with control or HBE1 siRNA and exposed to 5 Gy irradiation. Forty-eight hours later, the apoptotic rate was determined by FACS analysis based on annexin V staining. * p < 0.05, ** p < 0.01. (D) After exposure to radiation (5 Gy) for 24 h, cell cycle arrest at G2/M in SW480-IR and HT-29-IR cells transfected with control or HBE1 siRNA was analyzed by propidium iodide (PI) staining. All data shown are the means ± SD of three independent experiments.