HPV16 E7 protein antagonizes TNF-α-induced apoptosis of cervical cancer cells via Daxx/JNK pathway

被引:3
作者
Ding, Shuang [1 ,2 ]
Wang, Hanmeng [1 ]
Liao, Yaqi [1 ]
Chen, Ranzhong [1 ]
Hu, Yu [1 ]
Wu, Hongrong [1 ]
Shen, Haiyan [1 ]
Tang, Shuangyang [1 ]
机构
[1] Univ South China, Inst Pathogen Biol, Hengyang Med Coll, Sch Basic Med, Hengyang, Peoples R China
[2] Univ South China, Affiliated Hosp 7, Hunan Prov Vet Adm Hosp, Dept Clin Lab, Hengyang 421001, Hunan, Peoples R China
关键词
Human papillomavirus; HPV16; E7; Daxx; JNK; Interaction; Apoptosis; DOMAIN-ASSOCIATED PROTEIN; SUBCELLULAR-LOCALIZATION; HUMAN CYTOMEGALOVIRUS; INTERACTING PROTEIN; PROSTATE-CANCER; JNK; STRESS; DEATH; INHIBITION; ACTIVATION;
D O I
10.1016/j.micpath.2023.106423
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Human papillomavirus (HPV) E7 protein as an important viral factor was involved in the progression of cervical cancer by mediating the cellular signaling pathways. Daxx (Death domain-associated protein) can interact with a variety of proteins to affect the viral infection process. However, the interaction and its related function between HPV16 E7 and Daxx have not been adequately investigated. Here, it was found that HPV16 E7 can interact with Daxx in HeLa or C33A cells by co-immunoprecipitation. HPV16 E7 protein treatment can up-regulate Daxx protein expression, while the interference in Daxx expression and the agonists for JNK can both reduce the antagonistic effects of HPV16 E7 on TNF-alpha-induced apoptosis, suggesting that Daxx/JNK pathway may be involved in the anti-apoptotic activity of HPV16 E7.
引用
收藏
页数:10
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