Evidence map›Paper›PMID 38717113›Full record

ArticleJournal of virology2024

Degradation of TRIM32 is induced by RTA for Kaposi's sarcoma-associated herpesvirus lytic replication.

Yulin Zhang, Zhongwei Dong, Feng Gu, Yifei Xu, Ying Li, Wen Sun, Wutian Rao, Shujuan Du, Caixia Zhu, Yuyan Wang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of virology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Yulin Zhang *MOE/NHC/CAMS Key Laboratory of Medical Molecular Virology, Shanghai Institute of Infections Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganism and Infection, School of Basic Medical Science, Shanghai Medical College, Fudan University, Shanghai, China.
Zhongwei Dong *MOE/NHC/CAMS Key Laboratory of Medical Molecular Virology, Shanghai Institute of Infections Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganism and Infection, School of Basic Medical Science, Shanghai Medical College, Fudan University, Shanghai, China.
Feng Gu *MOE/NHC/CAMS Key Laboratory of Medical Molecular Virology, Shanghai Institute of Infections Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganism and Infection, School of Basic Medical Science, Shanghai Medical College, Fudan University, Shanghai, China.
Yifei Xu *MOE/NHC/CAMS Key Laboratory of Medical Molecular Virology, Shanghai Institute of Infections Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganism and Infection, School of Basic Medical Science, Shanghai Medical College, Fudan University, Shanghai, China.
Ying Li *MOE/NHC/CAMS Key Laboratory of Medical Molecular Virology, Shanghai Institute of Infections Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganism and Infection, School of Basic Medical Science, Shanghai Medical College, Fudan University, Shanghai, China.
Wen SunMOE/NHC/CAMS Key Laboratory of Medical Molecular Virology, Shanghai Institute of Infections Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganism and Infection, School of Basic Medical Science, Shanghai Medical College, Fudan University, Shanghai, China.
Wutian RaoMOE/NHC/CAMS Key Laboratory of Medical Molecular Virology, Shanghai Institute of Infections Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganism and Infection, School of Basic Medical Science, Shanghai Medical College, Fudan University, Shanghai, China.
Shujuan DuMOE/NHC/CAMS Key Laboratory of Medical Molecular Virology, Shanghai Institute of Infections Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganism and Infection, School of Basic Medical Science, Shanghai Medical College, Fudan University, Shanghai, China.
Caixia ZhuMOE/NHC/CAMS Key Laboratory of Medical Molecular Virology, Shanghai Institute of Infections Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganism and Infection, School of Basic Medical Science, Shanghai Medical College, Fudan University, Shanghai, China.
Yuyan WangMOE/NHC/CAMS Key Laboratory of Medical Molecular Virology, Shanghai Institute of Infections Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganism and Infection, School of Basic Medical Science, Shanghai Medical College, Fudan University, Shanghai, China.ORCID 0000-0002-1326-6831
Fang WeiShengYushou Center of Cell Biology and Immunology, Joint International Research Laboratory of Metabolic & Development Sciences, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, China.ORCID 0000-0001-8964-1645
Qiliang CaiMOE/NHC/CAMS Key Laboratory of Medical Molecular Virology, Shanghai Institute of Infections Disease and Biosecurity, Shanghai Frontiers Science Center of Pathogenic Microorganism and Infection, School of Basic Medical Science, Shanghai Medical College, Fudan University, Shanghai, China.ORCID 0000-0002-7147-0953

Funding

MOST | National Key Research and Development Program of China 2023YFC2306702, 2021YFA1300803MOST | National Natural Science Foundation of China (NSFC) 32120103001
6 · The paper itself

Abstract

TRIM32 is often aberrantly expressed in many types of cancers. Kaposi's sarcoma-associated herpesvirus (KSHV) is linked with several human malignancies, including Kaposi's sarcoma and primary effusion lymphomas (PELs). Increasing evidence has demonstrated the crucial role of KSHV lytic replication in viral tumorigenesis. However, the role of TRIM32 in herpesvirus lytic replication remains unclear. Here, we reveal that the expression of TRIM32 is upregulated by KSHV in latency, and reactivation of KSHV lytic replication leads to the inhibition of TRIM32 in PEL cells. Strikingly, RTA, the master regulator of lytic replication, interacts with TRIM32 and dramatically promotes TRIM32 for degradation via the proteasome systems. Inhibition of TRIM32 induces cell apoptosis and in turn inhibits the proliferation and colony formation of KSHV-infected PEL cells and facilitates the reactivation of KSHV lytic replication and virion production. Thus, our data imply that the degradation of TRIM32 is vital for the lytic activation of KSHV and is a potential therapeutic target for KSHV-associated cancers. IMPORTANCE: TRIM32 is associated with many cancers and viral infections; however, the role of TRIM32 in viral oncogenesis remains largely unknown. In this study, we found that the expression of TRIM32 is elevated by Kaposi's sarcoma-associated herpesvirus (KSHV) in latency, and RTA (the master regulator of lytic replication) induces TRIM32 for proteasome degradation upon viral lytic reactivation. This finding provides a potential therapeutic target for KSHV-associated cancers.

Indexed as

Herpesvirus 8, HumanImmediate-Early ProteinsProteolysisTrans-ActivatorsTranscription FactorsTripartite Motif ProteinsUbiquitin-Protein LigasesVirus ActivationVirus ReplicationApoptosisCell LineHumansLymphoma, Primary EffusionProteasome Endopeptidase ComplexSarcoma, KaposiVirus LatencyImmediate-Early ProteinsProteasome Endopeptidase ComplexRta protein, Human herpesvirus 8Trans-ActivatorsTranscription FactorsTRIM32 protein, humanTripartite Motif ProteinsUbiquitin-Protein LigasesKSHVlytic replicationRTATRIM32

Identifiers

PMID38717113
PMCPMC11237441

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.