Mitra Anirban Kumar, Krishna Malini
Radiation Biology and Health Sciences Division, Bhabha Atomic Research Centre, Trombay, Mumbai 400085, India.
J Cell Biochem. 2007 Jun 1;101(3):745-52. doi: 10.1002/jcb.21234.
The effect of fractionated doses of Co(60) gamma-irradiation (2 Gy per fraction over 5 days), as is delivered in cancer radiotherapy, was compared with acute doses of 10 and 2 Gy, in a serially transplanted mouse fibrosarcoma grown in Swiss mice. The aspects that were studied included the three major mitogen-activated protein (MAP) kinases, namely p44 MAP kinase, p38 MAP kinase, and stress-activated protein (SAP) kinase, which are known to be involved in determining the cell fate following exposure to ionizing radiation. The response of dual specificity phosphatase PAC1 which is involved in the dephosphorylation of MAP kinases was also looked at. There were significant differences in the response to different dose regimens for all the factors studied. Fractionated irradiation elicited an adaptive response with a sustained activation over 7 days of prosurvival p44 MAP kinase which was balanced by the increased activation of proapoptotic p54 SAP kinase up to 1 day post-irradiation, whereas, phosphorylated p38 MAP kinase showed a decrease at most time points. PAC1 was induced following fractionated irradiation and may be acting as a feed back regulator of p44 MAP kinase. The activation of SAP kinase after fractionated irradiation may be a stress response, whereas, constitutively activated p44 MAP kinase may play an important role in the induction of radioresistance during fractionated radiotherapy of cancer and may serve as a promising target for specific inhibitors to enhance the efficacy of radiotherapy.
将癌症放射治疗中给予的分次剂量钴(60)γ射线照射(5天内每次2 Gy)的效果,与10 Gy和2 Gy的急性剂量,在瑞士小鼠体内连续移植的小鼠纤维肉瘤中进行了比较。所研究的方面包括三种主要的丝裂原活化蛋白(MAP)激酶,即p44 MAP激酶、p38 MAP激酶和应激活化蛋白(SAP)激酶,已知它们参与决定细胞在受到电离辐射后的命运。还研究了参与MAP激酶去磷酸化的双特异性磷酸酶PAC1的反应。对于所有研究的因素,不同剂量方案的反应存在显著差异。分次照射引发了一种适应性反应,存活促进型p44 MAP激酶在7天内持续激活,这与促凋亡型p54 SAP激酶在照射后1天内激活增加相平衡,而磷酸化的p38 MAP激酶在大多数时间点显示下降。分次照射后诱导了PAC1,它可能作为p44 MAP激酶的反馈调节因子。分次照射后SAP激酶的激活可能是一种应激反应,而持续激活的p44 MAP激酶可能在癌症分次放射治疗期间的放射抗性诱导中起重要作用,并且可能作为增强放射治疗疗效的特异性抑制剂的有希望的靶点。