Evidence map›Paper›PMID 37989747›Full record

ArticleNature communications2023

SETD2 deficiency accelerates sphingomyelin accumulation and promotes the development of renal cancer.

Hanyu Rao, Changwei Liu, Aiting Wang, Chunxiao Ma, Yue Xu, Tianbao Ye, Wenqiong Su, Peijun Zhou, Wei-Qiang Gao, Li Li and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
9.7field-weighted citation impact, top 2% 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

31 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  7. Ribosome Homeostasis Regulated by SETD2 Preserves Intestinal Epithelial Barrier.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  8. Plasma lipidomics profiling to identify signatures of pediatric medulloblastoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  9. Article
  10. Article
  11. Loss of SETD2-mediated H3K36me3 Drives CD8Research (Washington, D.C.) · 2026
    Article
  12. Article
  13. Review
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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 1 institution in 1 country.

Hanyu RaoDepartment of Anesthesiology and Surgical Intensive Care Unit, Xinhua Hospital, School of Medicine and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Changwei LiuState Key Laboratory of Systems Medicine for Cancer, Institute for Personalized Medicine and Med-X Research Institute, Shanghai Jiao Tong University, Shanghai, China.
Aiting WangDepartment of Anesthesiology and Surgical Intensive Care Unit, Xinhua Hospital, School of Medicine and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Chunxiao MaState Key Laboratory of Systems Medicine for Cancer, Institute for Personalized Medicine and Med-X Research Institute, Shanghai Jiao Tong University, Shanghai, China.
Yue XuState Key Laboratory of Systems Medicine for Cancer, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, 200127, China.
Tianbao YeDepartment of Anesthesiology and Surgical Intensive Care Unit, Xinhua Hospital, School of Medicine and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Wenqiong SuDepartment of Anesthesiology and Surgical Intensive Care Unit, Xinhua Hospital, School of Medicine and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.ORCID 0000-0003-4914-346X
Peijun ZhouDivision of Kidney Transplant, Department of Urology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Wei-Qiang GaoState Key Laboratory of Systems Medicine for Cancer, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, 200127, China.ORCID 0000-0002-1989-4927
Li LiState Key Laboratory of Systems Medicine for Cancer, Institute for Personalized Medicine and Med-X Research Institute, Shanghai Jiao Tong University, Shanghai, China. lil@sjtu.edu.cn.ORCID 0000-0003-2342-3658
Xianting DingDepartment of Anesthesiology and Surgical Intensive Care Unit, Xinhua Hospital, School of Medicine and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China. dingxianting@sjtu.edu.cn.ORCID 0000-0002-1549-3499
Shanghai Jiao Tong University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 22077079National Natural Science Foundation of China (National Science Foundation of China) 82073104National Natural Science Foundation of China (National Science Foundation of China) 82203255National Natural Science Foundation of China (National Science Foundation of China) 82372604National Natural Science Foundation of China (National Science Foundation of China) T2122002
6 · The paper itself

Abstract

Patients with polycystic kidney disease (PKD) encounter a high risk of clear cell renal cell carcinoma (ccRCC), a malignant tumor with dysregulated lipid metabolism. SET domain-containing 2 (SETD2) has been identified as an important tumor suppressor and an immunosuppressor in ccRCC. However, the role of SETD2 in ccRCC generation in PKD remains largely unexplored. Herein, we perform metabolomics, lipidomics, transcriptomics and proteomics within SETD2 loss induced PKD-ccRCC transition mouse model. Our analyses show that SETD2 loss causes extensive metabolic reprogramming events that eventually results in enhanced sphingomyelin biosynthesis and tumorigenesis. Clinical ccRCC patient specimens further confirm the abnormal metabolic reprogramming and sphingomyelin accumulation. Tumor symptom caused by Setd2 knockout is relieved by myriocin, a selective inhibitor of serine-palmitoyl-transferase and sphingomyelin biosynthesis. Our results reveal that SETD2 deficiency promotes large-scale metabolic reprogramming and sphingomyelin biosynthesis during PKD-ccRCC transition. This study introduces high-quality multi-omics resources and uncovers a regulatory mechanism of SETD2 on lipid metabolism during tumorigenesis.

Indexed as

Carcinoma, Renal CellKidney NeoplasmsAnimalsCell Transformation, NeoplasticGenes, Tumor SuppressorHistone-Lysine N-MethyltransferaseHumansMiceSphingomyelinsHistone-Lysine N-MethyltransferaseSETD2 protein, mouseSphingomyelins

Identifiers

PMID37989747
PMCPMC10663509
OpenAlexW4388859671

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.