ArticleCell death and differentiation2019
Suppression of the SAP18/HDAC1 complex by targeting TRIM56 and Nanog is essential for oncogenic viral FLICE-inhibitory protein-induced acetylation of p65/RelA, NF-κB activation, and promotion of cell invasion and angiogenesis.
Article in Cell death and differentiation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 46 citations in OpenAlex.
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- miR-223-3p improves macrophage polarization balance and mitochondrial metabolism to ameliorate uveitis by orchestrating P65Cellular & molecular biology letters · 2026Article
- Mechanisms of Okanin against wound healing based on network pharmacology, molecular docking and molecular dynamics simulation.Scientific reports · 2025Article
- Tumor location, genomic alterations, and radiomic features as predictors of survival in glioblastoma: a Multi-Modal analysis.Neuroradiology · 2025Article
- Regulatory T Cell Infiltration-Driven Single-Cell Transcriptomic Analysis Identifies SAP18 as a Prognostic Marker for Esophageal Squamous Cell Carcinoma.Journal of gastrointestinal cancer · 2025Article
- TRIM56 Promotes White Adipose Tissue Browning to Attenuate Obesity by Degrading TLE3.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- HPV E6/E7-Induced Acetylation of a Peptide Encoded by a Long Non-Coding RNA Inhibits Ferroptosis to Promote the Malignancy of Cervical Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- HDAC1: a promising target for cancer treatment: insights from a thorough analysis of tumor functions.Translational cancer research · 2024Article
- Lactylation of RNA mProceedings of the National Academy of Sciences of the United States of America · 2024Article
- KSHV vIL-6 promotes SIRT3-induced deacetylation of SERBP1 to inhibit ferroptosis and enhance cellular transformation by inducing lipoyltransferase 2 mRNA degradation.PLoS pathogens · 2024Article
- Kaposi's sarcoma herpesvirus viral FLICE inhibitory protein modulates A20 deubiquitinase activity.Access microbiology · 2024Article
- Intricate confrontation: Research progress and application potential of TRIM family proteins in tumor immune escape.Journal of advanced research · 2023Review
- Immune evasion strategy involving propionylation by the KSHV interferon regulatory factor 1 (vIRF1).PLoS pathogens · 2023Article
- The Functions of TRIM56 in Antiviral Innate Immunity and Tumorigenesis.International journal of molecular sciences · 2023Review
- TRIM56 acts through the IQGAP1-CDC42 signaling axis to promote glioma cell migration and invasion.Cell death & disease · 2023Article
- TRIM56 promotes malignant progression of glioblastoma by stabilizing cIAP1 protein.Journal of experimental & clinical cancer research : CR · 2022Article
- A viral interferon regulatory factor degrades RNA-binding protein hnRNP Q1 to enhance aerobic glycolysis via recruiting E3 ubiquitin ligase KLHL3 and decaying GDPD1 mRNA.Cell death and differentiation · 2022Article
- Nm23-H1 induces apoptosis in primary effusion lymphoma cells via inhibition of NF-κB signaling through interaction with oncogenic latent protein vFLIP K13 of Kaposi's sarcoma-associated herpes virus.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Construction of a predictive model for immunotherapy efficacy in lung squamous cell carcinoma based on the degree of tumor-infiltrating immune cells and molecular typing.Journal of translational medicine · 2022Article
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Kaposi's sarcoma (KS), a highly invasive and angiogenic tumor of endothelial spindle-shaped cells, is the most common AIDS-associated cancer caused by KS-associated herpesvirus (KSHV) infection. KSHV-encoded viral FLICE-inhibitory protein (vFLIP) is a viral oncogenic protein, but its role in the dissemination and angiogenesis of KSHV-induced cancers remains unknown. Here, we report that vFLIP facilitates cell migration, invasion, and angiogenesis by downregulating the SAP18-HDAC1 complex. vFLIP degrades SAP18 through a ubiquitin-proteasome pathway by recruiting E3 ubiquitin ligase TRIM56. Further, vFLIP represses HDAC1, a protein partner of SAP18, by inhibiting Nanog occupancy on the HDAC1 promoter. Notably, vFLIP impairs the interaction between the SAP18/HDAC1 complex and p65 subunit, leading to enhancement of p65 acetylation and NF-κB activation. Our data suggest a novel mechanism of vFLIP activation of the NF-κB by decreasing the SAP18/HDAC1 complex to promote the acetylation of p65 subunit, which contributes to vFLIP-induced activation of the NF-κB pathway, cell invasion, and angiogenesis. These findings advance our understanding of the mechanism of KSHV-induced pathogenesis, and providing a rationale for therapeutic targeting of the vFLIP/SAP18/HDAC1 complex as a novel strategy of AIDS-KS.
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