کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1928448 | 1050355 | 2014 | 7 صفحه PDF | دانلود رایگان |
• Pre-treatment with the inhibitors increased the sensitivity of Jurkat cells to irradiation.
• Combining both inhibitors together resulted in a G2 cell cycle arrest abrogation in Jurkat.
• Jurkat cells pre-treated with inhibitors were positive for γH2AX foci 24 h upon irradiation.
• Pre-treatment with Rad51 RI-1 had no effect on apoptosis induction in MOLT-4 cells.
• When dosed together, the combination decreased MOLT-4 cell survival.
Present-day oncology sees at least two-thirds of cancer patients receiving radiation therapy as a part of their anticancer treatment. The objectives of the current study were to investigate the effects of the small molecule inhibitors of Wee1 kinase II (681641) and Rad51 (RI-1) on cell cycle progression, DNA double-strand breaks repair and apoptosis following ionizing radiation exposure in human leukemic T-cells Jurkat and MOLT-4. Pre-treatment with the Wee1 681641 or Rad51 RI-1 inhibitor alone increased the sensitivity of Jurkat cells to irradiation, however combining both inhibitors together resulted in a further enhancement of apoptosis. Jurkat cells pre-treated with inhibitors were positive for γH2AX foci 24 h upon irradiation. MOLT-4 cells were less affected by inhibitors application prior to ionizing radiation exposure. Pre-treatment with Rad51 RI-1 had no effect on apoptosis induction; however Wee1 681641 increased ionizing radiation-induced cell death in MOLT-4 cells.
Journal: Biochemical and Biophysical Research Communications - Volume 453, Issue 3, 24 October 2014, Pages 569–575