2017年 · 第37卷第01期

Recently, Tang Huangqi, Institute of Technical Biology and Agricultural Engineering, Hefei Institute of Physical Sciences, Chinese Academy of Sciences, and others, published in the official journal of the American Radiation AssociationRadiation Research(2016, 186:662 – 668, Impact Factor 3.022, DOI: 10.1667/RR14548.1) published the corresponding research paper "Interaction between radioadaptive response and radiation-induced bystander effect inCaenorhabditis elegans:A unique role of the DNA damage checkpoint ". In this paper, the author successfully demonstrated the adaptive response of radiation side-effect mediated cell proliferation and death at the individual level with the help of a living tissue model of proliferative death of vaginal cells of model organism nematodes, combined with single particle proton microbeam and gamma irradiation technology. In this paper, the authors first used single particle microbeams (1 000 and 2 000 protons) to precisely target the esophageal bulb and tail at both ends of the nematode body, and found that it can obviously induce the radiation resistance of vaginal cells located in the middle part of the nematode body, and reduce the rate of morphological malformations of the vagina caused by subsequent irradiation (100 Gy). Similarly, the use of microbeam irradiation to vulvar precursor cells of nematodes can also induce the radiation adaptive response of vulvar cells in situ. The authors also pointed out that the experimental model is not suitable for studying the effect of radiation adaptability on the side effect because the side effect of microbeam radiation itself cannot effectively induce the morphological distortion of the vulva. It is well known that DNA damage response plays an important role in regulating radiation side effects and adaptive responses. The results of nematode mutant analysis in this study show that DNA damage checkpoint and DNA damage non-homologous end junction (NHEJ) mechanism are involved in the adaptive response to radiation side effect-induced proliferation and death of columbial cells. However, it is interesting to note that only DNA repair mechanism activity but no DNA damage checkpoint mechanism activity exists in nematode columbial cells, suggesting that DNA damage checkpoints regulate side effects and in situ irradiation-induced columbial cell adaptive responses in a non-cell-autonomous manner. This discovery provides a new research idea for further clarifying the molecular mechanism of the correlation between radiation side effect and adaptive response. At the same time, considering the important influence of DNA damage response in the development and treatment of cancer, the elucidation of this molecular mechanism undoubtedly has important theoretical significance and potential application value for enhancing cancer radiotherapy.