标题：CD44 collaborates with ERBB2 mediate radiation resistance via p38 phosphorylation and DNA homologous recombination pathway in prostate cancer
作者：Ma, Ji-wei; Wang, Xiao; Chang, Lei; Zhong, Xue-yun; Jing, Haiyan; Zhu, Xiaolong; Wang, Shaoxiang; Xiao, WeiWei
作者机构：[Ma, Ji-wei; Jing, Haiyan] Shandong Univ, Shandong Prov Hosp, Dept Pathol, Jinan 250021, Shandong, Peoples R China.; [Xiao, WeiWei] Sun Yat Sen Univ 更多
通讯作者：Xiao, WW;Wang, SX
通讯作者地址：[Xiao, WW]Sun Yat Sen Univ, Dept Radiat Oncol, Ctr Canc, State Key Lab Oncol South China,Collaborat Innova, Guangzhou 510060, Guangdong, Peoples R Chi 更多
来源：ALCOHOL RESEARCH-CURRENT REVIEWS
关键词：CD44; ERBB2; p-p38; Homologous recombination; Prostate cancer
摘要：CD44, a glycoprotein, has been reported to have relationship with resistance to radiation in prostate cancer (Cap) cells. However, its molecular mechanism remains unknown. In this study, we demonstrated that inhibited CD44 enhanced the radiosentivity in Cap cells. It has been hypothesized that CD44 combine with ERBB2 and activate downstream phosphated protein to mediate DNA damage repair. Therefore, we conducted a detailed analysis of effects of radiation by clonogenic assay and immunofluorescence stain for p-H2AX foci. The downstream of CD44/ERBB2 and DNA damage repair proteins was detected by western blot. The results reveal that CD44 interacted with ERBB2, the downstream of CD44/ERBB2 was p-p38 when Cap cells were irradiated. Among the pathways, homologous recombination (HR) related proteins Mre11 and Rad50 were involved in CD44/ERBB2/p-p38 mediated radioresistance in Cap. In conclusion, CD44 could stabilize ERBB2 and co-activate p-p38 expression then promote the DNA damage repair by HR pathway, which finally contribute to the radio resistance of CaP.