The association of changes in RAD51 and survivin expression levels with the proton beam sensitivity of Capan‑1 and Panc‑1 human pancreatic cancer cells.

Abstract

Fewer than 20% of patients diagnosed with pancreatic cancer can be treated with surgical resection. The effects of proton beam irradiation were evaluated on the cell viabilities in Panc‑1 and Capan‑1 pancreatic cancer cells. The cells were irradiated with proton beams at the center of Bragg peaks with a 6‑cm width using a proton accelerator. Cell proliferation was assessed with the MTT assay, gene expression was analyzed with semi‑quantitative or quantitative reverse transcription‑polymerase chain reaction analyses and protein expression was evaluated by western blotting. The results demonstrated that Capan‑1 cells had lower cell viability than Panc‑1 cells at 72h after proton beam irradiation. Furthermore, the cleaved poly (ADP‑ribose) polymerase protein level was increased by irradiation in Capan‑1 cells, but not in Panc‑1 cells. Additionally, it was determined that histone H2AX phosphorylation in the two cell lines was increased by irradiation. Although a 16 Gy proton beam was only slightly up‑regulated cyclin‑dependent kinase inhibitor1 (p21) protein expression in Capan‑1 cells, p21 expression levels in Capan‑1 and Panc‑1 cells were significantly increased at 72h after irradiation. Furthermore, it was observed that the expression of DNA repair protein RAD51 homolog1 (RAD51), a homogenous repair enzyme, was decreased in what appeared to be a dose‑dependent manner by irradiation in Capan‑1 cells. Contrastingly, the transcription of survivin in Panc‑1 was significantly enhanced. The results suggest that RAD51 and survivin are potent markers that determine the therapeutic efficacy of proton beam therapy in patients with pancreatic cancer.