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E2F is involved in radioresistance of carbon ion induced apoptosis via Bax/caspase 3 signal pathway in human hepatoma cell
Author(s) -
Xie Yi,
Si Jing,
Wang YuPei,
Li HongYan,
Di CuiXia,
Yan JunFang,
Ye YanCheng,
Zhang YanShan,
Zhang Hong
Publication year - 2018
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.26005
Subject(s) - radioresistance , apoptosis , cancer research , clonogenic assay , cell cycle , e2f1 , cancer cell , mdm2 , biology , signal transduction , programmed cell death , microbiology and biotechnology , cell , chemistry , cancer , cell culture , biochemistry , genetics
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.