Evidence map›Paper›PMID 40470795›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Lipid Droplet-Organized MDM2-Mediated P53 Degradation: A Metabolic Switch Governing Diet-Driven Tumor Progression.

Haiyang Liu, Lin Jing, Yixin Li, Jinxing Zhou, Xiaohui Cui, Sen Li, Shijie Yang, Fangming Kan, Junfeng Du, Wentao Zhong and 11 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
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

21 authors.

Haiyang LiuDepartment of General Surgery, Pancreatic Disease Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.ORCID https://orcid.org/0009-0002-0838-2253
Lin JingCAS Engineering Laboratory for Nanozyme, Key Laboratory of Biomacromolecules (CAS), CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, PR China.
Yixin LiUniversity of Chinese Academy of Sciences, Beijing, 100049, China.
Jinxing ZhouNational Institute of Biological Sciences, Beijing, 102206, China.
Xiaohui CuiSchool of Information Science and Technology, Beijing Forestry University, Beijing, 100083, China.
Sen LiDepartment of Biochemistry & Immunology, Capital Institute of Pediatrics, Beijing, 100020, China.
Shijie YangSchool of Information Science and Technology, Beijing Forestry University, Beijing, 100083, China.
Fangming KanUniversity of Chinese Academy of Sciences, Beijing, 100049, China.
Junfeng DuMedical Department of General Surgery, The 1st Medical Center, Chinese PLA General Hospital, Beijing, 100853, China.
Wentao ZhongThe Second School of Clinical Medicine, Southern Medical University, Guangzhou, 510515, China.
Sheng YuUniversity of Chinese Academy of Sciences, Beijing, 100049, China.
Ning WangUniversity of Chinese Academy of Sciences, Beijing, 100049, China.
Xing JiaCenter for Biological Imaging, Core Facilities for Protein Science, Institute of Biophysics, CAS, Beijing, 100101, China.
Junhui LiUniversity of Chinese Academy of Sciences, Beijing, 100049, China.
Pan NieUniversity of Chinese Academy of Sciences, Beijing, 100049, China.
Zhenzhong ChenUniversity of Chinese Academy of Sciences, Beijing, 100049, China.
Ying HanUniversity of Chinese Academy of Sciences, Beijing, 100049, China.
Lingxi JiangDepartment of General Surgery, Pancreatic Disease Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Xiyun YanCAS Engineering Laboratory for Nanozyme, Key Laboratory of Biomacromolecules (CAS), CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, PR China.
Hongxia DuanCAS Engineering Laboratory for Nanozyme, Key Laboratory of Biomacromolecules (CAS), CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, PR China.
Baiyong ShenDepartment of General Surgery, Pancreatic Disease Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.

Funding

Beijing Natural Science Foundation of China 7242092Beijing Natural Science Foundation of China L232077Major Program of Nanozyme Laboratory in Zhongyuan NLZ-MP2024BIC01National Natural Science Foundation of China 82203559National Natural Science Foundation of China 82402154
6 · The paper itself

Abstract

TP53 inactivation in human cancers often results from MDM2/MDMX overexpression, yet therapeutic targeting remains challenging owing to incomplete mechanistic understanding. Lipid droplet (LD) enrichment is identified as a key trigger for MDM2-mediated p53 degradation. High-fat diet (HFD)-induced LD accumulation in tumor cells elevates LD-surface MDM2 through Cyb5r3-Myh9 interactions, which recruit cytoplasmic p53/Myh9 complexes to LDs. This spatial proximity enhances MDM2-p53 binding, accelerating its ubiquitination and proteasomal degradation. Degraded p53 releases the RPS3A-C/EBPβ complex, upregulating LD-promoting factors such as CD36 to establish a cell-autonomous feed-forward loop. Critically, pharmacological LD reduction (via lipogenesis inhibitors) or switching of tumor-bearing mice from an HFD to a normal diet restores p53 levels and suppresses tumor growth. These findings delineate a lipid-driven regulatory axis in which LD biogenesis initiates MDM2-dependent p53 destruction, reshaping tumor cell lipid metabolism. This mechanism links dietary lipids to oncogenesis through organelle-specific protein trafficking and provides a therapeutic rationale for targeting lipid metabolism in tumors. This study resolves critical gaps in p53 regulation while proposing dual intervention strategies: disrupting LD-MDM2 colocalization and modulating lipid availability.

Indexed as

Diet, High-FatLipid DropletsNeoplasmsProto-Oncogene Proteins c-mdm2AnimalsCell Line, TumorDisease ProgressionFemaleHumansHypertriglyceridemiaMiceTumor Suppressor Protein p53Proto-Oncogene Proteins c-mdm2Tumor Suppressor Protein p53high‐fat dietslipid dropletsp53 degradation initiationtumor growth

Identifiers

PMID40470795
PMCPMC12407345

What Socratic 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 Socratic graph.