Evidence map›Paper›PMID 38470932›Full record

ArticlePLoS pathogens2024

KSHV vIL-6 promotes SIRT3-induced deacetylation of SERBP1 to inhibit ferroptosis and enhance cellular transformation by inducing lipoyltransferase 2 mRNA degradation.

Jing Zhou, Tianjiao Wang, Haoran Zhang, Jianhong Liu, Pengjun Wei, Ruoqi Xu, Qin Yan, Guochun Chen, Wan Li, Shou-Jiang Gao and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.0field-weighted citation impact, top 6% of its field
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

13 citing papers in PubMed, 14 citations in OpenAlex.

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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

11 authors at 3 institutions in 2 countries.

Jing ZhouDepartment of Microbiology, Nanjing Medical University, Nanjing, People's Republic of China.ORCID 0000-0002-6078-9352
Tianjiao WangDepartment of Microbiology, Nanjing Medical University, Nanjing, People's Republic of China.
Haoran ZhangDepartment of Microbiology, Nanjing Medical University, Nanjing, People's Republic of China.
Jianhong LiuDepartment of Pathology, Changzhou Third People's Hospital, Changzhou, People's Republic of China.
Pengjun WeiDepartment of Microbiology, Nanjing Medical University, Nanjing, People's Republic of China.
Ruoqi XuDepartment of Microbiology, Nanjing Medical University, Nanjing, People's Republic of China.
Qin YanDepartment of Microbiology, Nanjing Medical University, Nanjing, People's Republic of China.
Guochun ChenDepartment of Infectious Diseases, Changzhou Third People's Hospital, Changzhou, People's Republic of China.
Wan LiDepartment of Microbiology, Nanjing Medical University, Nanjing, People's Republic of China.
Shou-Jiang GaoTumor Virology Program, UPMC Hillman Cancer Center, and Department of Microbiology and Molecular Genetics, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Chun LuDepartment of Microbiology, Nanjing Medical University, Nanjing, People's Republic of China.ORCID 0000-0002-6078-9352
Nanjing Medical University · CNChangzhou Third People's Hospital · CNUPMC Hillman Cancer Center · US

Funding

KSHV microRNAs in tumor invasion and angiogenesisR01CA213275 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GAO, SHOU-JIANG · 2017 to 2021
$959k
NCI NIH HHS R01 CA213275
6 · The paper itself

Abstract

Ferroptosis, a defensive strategy commonly employed by the host cells to restrict pathogenic infections, has been implicated in the development and therapeutic responses of various types of cancer. However, the role of ferroptosis in oncogenic Kaposi's sarcoma-associated herpesvirus (KSHV)-induced cancers remains elusive. While a growing number of non-histone proteins have been identified as acetylation targets, the functions of these modifications have yet to be revealed. Here, we show KSHV reprogramming of host acetylation proteomics following cellular transformation of rat primary mesenchymal precursor. Among them, SERPINE1 mRNA binding protein 1 (SERBP1) deacetylation is increased and required for KSHV-induced cellular transformation. Mechanistically, KSHV-encoded viral interleukin-6 (vIL-6) promotes SIRT3 deacetylation of SERBP1, preventing its binding to and protection of lipoyltransferase 2 (Lipt2) mRNA from mRNA degradation resulting in ferroptosis. Consequently, a SIRT3-specific inhibitor, 3-TYP, suppresses KSHV-induced cellular transformation by inducing ferroptosis. Our findings unveil novel roles of vIL-6 and SERBP1 deacetylation in regulating ferroptosis and KSHV-induced cellular transformation, and establish the vIL-6-SIRT3-SERBP1-ferroptosis pathways as a potential new therapeutic target for KSHV-associated cancers.

Indexed as

FerroptosisHerpesvirus 8, HumanNeoplasmsSarcoma, KaposiSirtuin 3AnimalsCell Transformation, NeoplasticRatsRNA, MessengerViral ProteinsRNA, MessengerSirtuin 3Viral Proteins

Identifiers

PMID38470932
PMCPMC10959363
OpenAlexW4392696837

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.