ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2014
HIV-1 viral protein R downregulates Ebp1 and stabilizes p53 in glioblastoma U87MG cells.
Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- Targeted protein degradation: from mechanisms to clinic.Nature reviews. Molecular cell biology · 2024Review
- Comparative Analysis of Differential Cellular Transcriptome and Proteome Regulation by HIV-1 and HIV-2 Pseudovirions in the Early Phase of Infection.International journal of molecular sciences · 2023Article
- Proteomics Profiling of Host Cell Response via Protein Expression and Phosphorylation upon Dengue Virus Infection.Virologica Sinica · 2019Article
- HIV-1 Gp120 clade B/C induces a GRP78 driven cytoprotective mechanism in astrocytoma.Oncotarget · 2017Article
- Article
- Cullin E3 ligases and their rewiring by viral factors.Biomolecules · 2014Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeHIV-1 viral protein R (Vpr) inhibits cell growth and induces apoptosis in a wide range of cancers. However, the mechanism by which Vpr induces cell cycle arrest and apoptosis in GBM cell lines is unclear. The present work was taken to detect the proteins interacted with Vpr in U87MG cells.
methodsWe analyzed the differential expression of proteins between glioblastoma cell U87MG treated with Ad-Vpr and untreated by 2-DE. We used antibody array analysis to analyze the common molecules in the apoptosis of U87MG induced by Vpr.
resultsWe analyzed the differential expression of proteins between U87MG cell treated with Ad-Vpr and untreated, and found that proteins related to DNA damage repair or different apoptosis pathways were involved in the G2 arrest and apoptosis mediated by Vpr. In addition, proliferation-associated protein 2G4 (PA2G4), also known as Ebp1, was down-regulated and p53 was up-regulated in U87MG cells treated with Ad-Vpr.
conclusionsOur data suggest that Vpr may inhibit Ebp1 to stabilize p53, which in turn leads to G2 arrest and apoptosis in U87MG cells.
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