HPV16 E7 蛋白通过 Daxx/JNK 通路拮抗 TNF-α 诱导的宫颈癌细胞凋亡。

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

机构信息

Institute of Pathogenic Biology, School of Basic Medicine Sciences, Hengyang Medical College, University of South China, Hengyang, China; Department of Clinical Laboratory, The Seventh Affiliated Hospital, University of South China / Hunan Provincial Veterans Administration Hospital, Changsha, China.

Institute of Pathogenic Biology, School of Basic Medicine Sciences, Hengyang Medical College, University of South China, Hengyang, China.

出版信息

Microb Pathog. 2023 Dec;185:106423. doi: 10.1016/j.micpath.2023.106423. Epub 2023 Oct 21.

DOI:10.1016/j.micpath.2023.106423

PMID:37871853

Abstract

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-α-induced apoptosis, suggesting that Daxx/JNK pathway may be involved in the anti-apoptotic activity of HPV16 E7.

摘要

人乳头瘤病毒（HPV）E7 蛋白作为一种重要的病毒因子，通过介导细胞信号通路参与宫颈癌的进展。Daxx（死亡结构域相关蛋白）可以与多种蛋白质相互作用，影响病毒感染过程。然而，HPV16 E7 和 Daxx 之间的相互作用及其相关功能尚未得到充分研究。在这里，通过共免疫沉淀发现 HPV16 E7 可以与 HeLa 或 C33A 细胞中的 Daxx 相互作用。HPV16 E7 蛋白处理可以上调 Daxx 蛋白表达，而 Daxx 表达的干扰和 JNK 的激动剂均可降低 HPV16 E7 对 TNF-α诱导的细胞凋亡的拮抗作用，提示 Daxx/JNK 通路可能参与 HPV16 E7 的抗凋亡活性。