Published online Aug 14, 2017. doi: 10.3748/wjg.v23.i30.5530
Peer-review started: March 17, 2017
First decision: May 16, 2017
Revised: May 26, 2017
Accepted: July 4, 2017
Article in press: July 4, 2017
Published online: August 14, 2017
Processing time: 151 Days and 4.5 Hours
To investigate whether autophagic cell death is involved in hyperthermic sensitization to ionizing radiation in human hepatocellular carcinoma cells, and to explore the underlying mechanism.
Human hepatocellular carcinoma cells were treated with hyperthermia and ionizing radiation. MTT and clonogenic assays were performed to determine cell survival. Cell autophagy was detected using acridine orange staining and flow cytometric analysis, and the expression of autophagy-associated proteins, LC3 and p62, was determined by Western blot analysis. Intracellular reactive oxygen species (ROS) were quantified using the fluorescent probe DCFH-DA.
Treatment with hyperthermia and ionizing radiation significantly decreased cell viability and surviving fraction as compared with hyperthermia or ionizing radiation alone. Cell autophagy was significantly increased after ionizing radiation combined with hyperthermia treatment, as evidenced by increased formation of acidic vesicular organelles, increased expression of LC3II and decreased expression of p62. Intracellular ROS were also increased after combined treatment with hyperthermia and ionizing radiation. Pretreatment with N-acetylcysteine, an ROS scavenger, markedly inhibited the cytotoxicity and cell autophagy induced by hyperthermia and ionizing radiation.
Autophagic cell death is involved in hyperthermic sensitization of cancer cells to ionizing radiation, and its induction may be due to the increased intracellular ROS.
Core tip: Increased cell autophagy and intracellular reactive oxygen species (ROS), accompanied by decreased cell viability and surviving fraction, were observed in HepG2 cells treated with hyperthermia and ionizing radiation. Pretreatment with N-acetylcysteine, an ROS scavenger, markedly inhibited the above cytotoxicity and cell autophagy. The results suggest that autophagic cell death is involved in the hyperthermic sensitization to ionizing radiation, and its induction may be due to the increased intracellular ROS.