Evidence map›Paper›PMID 39971971›Full record

ArticleNature communications2025

Lipogenic enzyme FASN promotes mutant p53 accumulation and gain-of-function through palmitoylation.

Juan Liu, Yiyun Shen, Jie Liu, Dandan Xu, Chun-Yuan Chang, Jianming Wang, Jason Zhou, Bruce G Haffty, Lanjing Zhang, Jill Bargonetti and 3 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

  1. Review
  2. Revisiting tumor immunogenicity through the lens of mutant p53: Implications for cancer immunotherapy.Apoptosis : an international journal on programmed cell death · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. S-palmitoylation in ferroptosis: molecular mechanisms, modulators, and interplay with autophagy.Apoptosis : an international journal on programmed cell death · 2026
    Review
  18. Review
  19. Article
  20. 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

13 authors.

Juan LiuDepartment of Radiation Oncology, Rutgers Cancer Institute, Rutgers-State University of New Jersey, New Brunswick, NJ, USA.
Yiyun ShenDepartment of Radiation Oncology, Rutgers Cancer Institute, Rutgers-State University of New Jersey, New Brunswick, NJ, USA.
Jie LiuDepartment of Radiation Oncology, Rutgers Cancer Institute, Rutgers-State University of New Jersey, New Brunswick, NJ, USA.
Dandan XuDepartment of Radiation Oncology, Rutgers Cancer Institute, Rutgers-State University of New Jersey, New Brunswick, NJ, USA.
Chun-Yuan ChangDepartment of Radiation Oncology, Rutgers Cancer Institute, Rutgers-State University of New Jersey, New Brunswick, NJ, USA.
Jianming WangDepartment of Radiation Oncology, Rutgers Cancer Institute, Rutgers-State University of New Jersey, New Brunswick, NJ, USA.
Jason ZhouDepartment of Radiation Oncology, Rutgers Cancer Institute, Rutgers-State University of New Jersey, New Brunswick, NJ, USA.
Bruce G HafftyDepartment of Radiation Oncology, Rutgers Cancer Institute, Rutgers-State University of New Jersey, New Brunswick, NJ, USA.
Lanjing ZhangDepartment of Pathology, Princeton Medical Center, Princeton, NJ, USA.
Jill BargonettiDepartment of Biological Sciences, Hunter College, City University of New York, New York, NY, USA.ORCID http://orcid.org/0000-0003-2692-0991
Subhajyoti DeCenter for Systems and Computational Biology, Rutgers Cancer Institute, Rutgers-State University of New Jersey, New Brunswick, NJ, USA.ORCID http://orcid.org/0000-0002-2313-8593
Wenwei HuDepartment of Radiation Oncology, Rutgers Cancer Institute, Rutgers-State University of New Jersey, New Brunswick, NJ, USA. wh221@cinj.rutgers.edu.ORCID http://orcid.org/0000-0003-3971-4257
Zhaohui FengDepartment of Radiation Oncology, Rutgers Cancer Institute, Rutgers-State University of New Jersey, New Brunswick, NJ, USA. fengzh@cinj.rutgers.edu.ORCID http://orcid.org/0000-0002-8912-6456

Funding

Gain-of-function mutant p53 and metabolic reprogramming in colorectal cancerR01CA260837 · NCI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI FENG, ZHAOHUI, HU, WENWEI · 2021 to 2025
$2.2M
The regulation of mutant p53 protein accumulation in cancer: molecular basis and therapeutic potentialR01CA229257 · NCI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI FENG, ZHAOHUI · 2021 to 2025
$2.0M
The role of chronic stress in regulation of mutant p53 and tumorigenesisR01CA203965 · NCI · RBHS -CANCER INSTITUTE OF NEW JERSEY · PI HU, WENWEI · 2017 to 2021
$1.8M
SENP6, a novel p53 negative regulator, is an important new player in cancerR01CA214746 · NCI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI FENG, ZHAOHUI · 2018 to 2022
$1.8M
NCI NIH HHS R01 CA203965NCI NIH HHS R01 CA214746NCI NIH HHS R01 CA229257NCI NIH HHS R01 CA260837U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA214746U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA229257
6 · The paper itself

Abstract

The tumor-suppressive function of p53 is frequently disrupted by mutations in cancers. Missense mutant p53 (mutp53) protein often stabilizes and accumulates to high levels in cancers to promote tumorigenesis through the gain-of-function (GOF) mechanism. Currently, the mechanism of mutp53 accumulation and GOF is incompletely understood. Here, we identify the lipogenic enzyme FASN as an important regulator of mutp53 accumulation and GOF. FASN interacts with mutp53 to enhance mutp53 palmitoylation, which inhibits mutp53 ubiquitination to promote mutp53 accumulation and GOF. Blocking FASN genetically or by small-molecule inhibitors suppresses mutp53 palmitoylation to inhibit mutp53 accumulation, which in turn inhibits the growth of mutp53 tumors in orthotopic and subcutaneous xenograft tumor models and transgenic mice, as well as the growth of human tumor organoids carrying mutp53. Our results reveal that mutp53 palmitoylation is an important mechanism underlying mutp53 accumulation and GOF, and targeting FASN is a potential therapeutic strategy for cancers carrying mutp53.

Indexed as

Fatty Acid Synthase, Type IGain of Function MutationLipoylationTumor Suppressor Protein p53AnimalsCell Line, TumorFemaleHEK293 CellsHumansLipogenesisMiceMice, TransgenicUbiquitinationXenograft Model Antitumor AssaysFASN protein, humanFatty Acid Synthase, Type ITP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID39971971
PMCPMC11839913

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.