E2F is involved in radioresistance of carbon ion induced apoptosis via Bax/caspase 3 signal pathway in human hepatoma cell

doi:10.1002/jcp.26005

	E2F is involved in radioresistance of carbon ion induced apoptosis via Bax/caspase 3 signal pathway in human hepatoma cell
	Xie, Yi1,2,3 ; Si, Jing1,2,3 ; Wang, Yu-Pei 1,2,3,4; Li, Hong-Yan 1,2,3,4; Di, Cui-Xia1,2,3 ; Yan, Jun-Fang 1,2,3,4; Ye, Yan-Cheng 5; Zhang, Yan-Shan 5; Zhang, Hong1,2,3,5
刊名	JOURNAL OF CELLULAR PHYSIOLOGY
	2018-02-01
卷号	233 期号:2 页码:1312-1320
关键词	apoptosis cancer cells carbon ion irradiation E2F1 radioresistance
ISSN号	0021-9541
DOI	10.1002/jcp.26005
英文摘要	Deletion of p53, most common genetic alteration, is observed in human tumors and reported to lead to improve in cell radioresistance. Heavy-ion irradiation (IR) could induce p53(-/-) cancer cells apoptosis. However, little is known regarding the molecular mechanism in this type of cell apoptosis. The present studies have focused on mechanisms state of signaling pathways as an activator of the cell fate decisions induced by heavy ion IR without p53. Carbon ion IR could induce up-regulation of E2F1 expression in cancer cells. This phenomenon was not observed in X-ray IR group. Up-regulation of E2F1 could cause a higher reduction in clonogenic survival, low level of cellular activity, G(2)/M phase arrest, promotion of apoptosis rate, up-regulation of phosphor-Rb, Bax, and cleaved-caspase 3 proteins expressions without p53. Changes of E2F1 expressions could partly alter radioresistance in cancer cells. The results were suggested that heavy ion IR could induce p53(-/-) cancer cells apoptosis via E2F1 signal pathway. Our study provides a scientific rationale for the clinical use of heavy ion as radiotherapy in patients with p53-deficient tumors, which are often resistant to radiotherapy.
资助项目	Key Program of National Natural Science Foundation of China[U1432248] ; Ministry of Science and Technology National Key R D Project[2016YFC0904600] ; Western Talent Program of Chinese Academy of Sciences ; National Natural Science Foundation of China[11605260]
WOS关键词	HUMAN HEPATOCELLULAR-CARCINOMA ; DNA-DAMAGE ; RETINOBLASTOMA GENE ; IONIZING-RADIATION ; TUMOR-SUPPRESSOR ; P53 ; RESISTANCE ; CANCER ; HEAD ; TRANSLOCATION
WOS研究方向	Cell Biology ; Physiology
语种	英语
出版者	WILEY
WOS记录号	WOS:000414593500052
资助机构	Key Program of National Natural Science Foundation of China ; Ministry of Science and Technology National Key R D Project ; Western Talent Program of Chinese Academy of Sciences ; National Natural Science Foundation of China
内容类型	期刊论文
源URL	[http://119.78.100.186/handle/113462/45903]
专题	中国科学院近代物理研究所
通讯作者	Zhang, Hong
作者单位	1.Chinese Acad Sci, Inst Modern Phys, 509 Nanchang Rd, Lanzhou 730000, Peoples R China 2.Inst Modern Phys, CAS Key Lab Heavy Ion Radiat Biol & Med, Lanzhou, Gansu, Peoples R China 3.Key Lab Basic Res Heavy Ion Radiat Applicat Med, Lanzhou, Gansu, Peoples R China 4.Univ Chinese Acad Sci, Grad Sch, Beijing, Peoples R China 5.Gansu Wuwei Tumor Hosp, Wuwei, Peoples R China
推荐引用方式 GB/T 7714	Xie, Yi,Si, Jing,Wang, Yu-Pei,et al. E2F is involved in radioresistance of carbon ion induced apoptosis via Bax/caspase 3 signal pathway in human hepatoma cell[J]. JOURNAL OF CELLULAR PHYSIOLOGY,2018,233(2):1312-1320.
APA	Xie, Yi.,Si, Jing.,Wang, Yu-Pei.,Li, Hong-Yan.,Di, Cui-Xia.,...&Zhang, Hong.(2018).E2F is involved in radioresistance of carbon ion induced apoptosis via Bax/caspase 3 signal pathway in human hepatoma cell.JOURNAL OF CELLULAR PHYSIOLOGY,233(2),1312-1320.
MLA	Xie, Yi,et al."E2F is involved in radioresistance of carbon ion induced apoptosis via Bax/caspase 3 signal pathway in human hepatoma cell".JOURNAL OF CELLULAR PHYSIOLOGY 233.2(2018):1312-1320.