There are many fuctions with the representative autophagy associated protein p62,such as cell signal transduction,cell proliferation,apoptosis,inflammation,tumorigenesis and oxidative stress.p62 over express will lead...There are many fuctions with the representative autophagy associated protein p62,such as cell signal transduction,cell proliferation,apoptosis,inflammation,tumorigenesis and oxidative stress.p62 over express will lead to autophagy disorder by controlling keap1-Nrf2mTORC1,NF-κB signaling pathways,thus promoting the development of the tumor.The overexpression of p62 in tissues can lead to the occurrence of the gynecological malignant tumors,such as ceicival cancer,ovarian carcinoma and Endometrial carcinoma.And the level of p62 is correlated with the tumor progression,the tumor grade and the survival rates of patients.p62 and its upstream and downstream molecules are expected to be the markers and therapeutic targets for predicting the clinical outcome of the gynecological malignant cancer patients.展开更多
Viral protein R(Vpr) plays an important role in the replication and pathogenesis of Human immunodeficiency virus type 1(HIV-1). Some of the various functions attributed to Vpr, including the induction of G2/M cell cyc...Viral protein R(Vpr) plays an important role in the replication and pathogenesis of Human immunodeficiency virus type 1(HIV-1). Some of the various functions attributed to Vpr, including the induction of G2/M cell cycle arrest, activating the NF-κB pathway, and promoting viral reverse transcription, might be interrelated. To test this hypothesis, a panel of Vpr mutants were investigated for their ability to induce G2/M arrest and to activate the NF-κB pathway. The results showed that the Vpr mutants that failed to activate NF-κB also lost the activity to induce G2/M arrest, which suggests that inducing G2/M arrest via Vpr depends at least partially on the activation of NF-κB. This latter possibility is supported by data showing that knocking down the key factors in the NF-κB pathway – p65, Rel B, IKKα, or IKKβ– partially rescued the G2/M arrest induced by Vpr.Our results suggest that the NF-κB pathway is probably involved in Vpr-induced G2/M cell cycle arrest.展开更多
基金Key Research and Development program of Shanxi Province(No.201903D421065)Shanxi Health Commission(No.201601046)PhD Foundation of Shanxi Medical University Second Affiliated Hospital(No.201701-8)
文摘There are many fuctions with the representative autophagy associated protein p62,such as cell signal transduction,cell proliferation,apoptosis,inflammation,tumorigenesis and oxidative stress.p62 over express will lead to autophagy disorder by controlling keap1-Nrf2mTORC1,NF-κB signaling pathways,thus promoting the development of the tumor.The overexpression of p62 in tissues can lead to the occurrence of the gynecological malignant tumors,such as ceicival cancer,ovarian carcinoma and Endometrial carcinoma.And the level of p62 is correlated with the tumor progression,the tumor grade and the survival rates of patients.p62 and its upstream and downstream molecules are expected to be the markers and therapeutic targets for predicting the clinical outcome of the gynecological malignant cancer patients.
基金supported by grants from the Chinese Ministry of Health (2012ZX10001006)the National Natural Science Foundation of China (81271812 and 31370182)+1 种基金111 Project (B08011)the Postgraduate Scholarship Program of the China Scholarship Council
文摘Viral protein R(Vpr) plays an important role in the replication and pathogenesis of Human immunodeficiency virus type 1(HIV-1). Some of the various functions attributed to Vpr, including the induction of G2/M cell cycle arrest, activating the NF-κB pathway, and promoting viral reverse transcription, might be interrelated. To test this hypothesis, a panel of Vpr mutants were investigated for their ability to induce G2/M arrest and to activate the NF-κB pathway. The results showed that the Vpr mutants that failed to activate NF-κB also lost the activity to induce G2/M arrest, which suggests that inducing G2/M arrest via Vpr depends at least partially on the activation of NF-κB. This latter possibility is supported by data showing that knocking down the key factors in the NF-κB pathway – p65, Rel B, IKKα, or IKKβ– partially rescued the G2/M arrest induced by Vpr.Our results suggest that the NF-κB pathway is probably involved in Vpr-induced G2/M cell cycle arrest.
