Evidence map›Paper›PMID 40051297›Full record

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

PDCD11 Stabilizes C-MYC Oncoprotein by Hindering C-MYC-SKP2 Negative Feedback Loop to Facilitate Progression of p53-Mutant Breast and Colon Malignancies.

Li Ding, Wei Ni, Yichao Ma, Lin Xu, Zhiping Zhang, Kai Liao, Jingwen Li, Xinyu Mei, Zhun Wang, Huiqian Ge and 3 more

Abstract read
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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 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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

13 authors.

Li DingCollege of Bioscience and Biotechnology, Yangzhou University, Yangzhou, 225009, China.ORCID https://orcid.org/0000-0002-6244-1683
Wei NiCollege of Bioscience and Biotechnology, Yangzhou University, Yangzhou, 225009, China.
Yichao MaDepartment of General Surgery, Institute of General Surgery, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou, 225001, China.
Lin XuCollege of Bioscience and Biotechnology, Yangzhou University, Yangzhou, 225009, China.
Zhiping ZhangCollege of Bioscience and Biotechnology, Yangzhou University, Yangzhou, 225009, China.
Kai LiaoCollege of Bioscience and Biotechnology, Yangzhou University, Yangzhou, 225009, China.
Jingwen LiCollege of Bioscience and Biotechnology, Yangzhou University, Yangzhou, 225009, China.
Xinyu MeiCollege of Bioscience and Biotechnology, Yangzhou University, Yangzhou, 225009, China.
Zhun WangCollege of Bioscience and Biotechnology, Yangzhou University, Yangzhou, 225009, China.
Huiqian GeCollege of Bioscience and Biotechnology, Yangzhou University, Yangzhou, 225009, China.
Jiajia LiCollege of Bioscience and Biotechnology, Yangzhou University, Yangzhou, 225009, China.
Dong TangDepartment of General Surgery, Institute of General Surgery, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou, 225001, China.
Xinyue ZhangCollege of Bioscience and Biotechnology, Yangzhou University, Yangzhou, 225009, China.

Funding

Jiangsu Provincial Department of Science and Technology BE2022773Natural Science Foundation of China 81802765Natural Science Foundation of Jiangsu Province BK20160478Postgraduate Research & Practice Innovation Program of Jiangsu Province SJCX24_2324Six Talent Peaks Project in Jiangsu Province 2014-SWYY-016
6 · The paper itself

Abstract

C-MYC is a proto-oncoprotein whose dysregulation triggers tumorigenesis and tumor progression in ≈70% of cancer cases. It is presently demonstrated that aberrantly upregulated MYC is caused by the overexpressed and "extra-nucleolar" PDCD11 in p53-mutant breast and colon cancer cells, which is highly correlated to tumor progression, metastasis, and recurrence. In the nucleoplasm, PDCD11 binds to the TAD of C-MYC to prevent SKP2, a transcriptional target of C-MYC as well as one of the major E3 ligase components targeting C-MYC, from interacting with and ubiquitinating C-MYC in feedback. The ensuing stabilized C-MYC activates downstream signaling to facilitate the cellular G1/S transition, proliferation, and migration. PDCD11 silencing restores SKP2-mediated C-MYC degradation, thereby remarkably suppressing tumor growth and metastasis in nude mice. These findings highlight PDCD11 as a novel C-MYC partner and thereby offer a potential therapeutic rationale to challenge PDCD11-mediated "pro-stabilization" effect on C-MYC, a widely considered "undruggable" target, to combat C-MYC-driven malignancies with p53 mutation.

Indexed as

Apoptosis Regulatory ProteinsBreast NeoplasmsColonic NeoplasmsProto-Oncogene Proteins c-mycTumor Suppressor Protein p53AnimalsCell Line, TumorCell ProliferationDisease ProgressionFemaleHumansMiceMice, NudeApoptosis Regulatory ProteinsMYC protein, humanProto-Oncogene Proteins c-mycTP53 protein, humanTumor Suppressor Protein p53C‐MYCp53‐mutant breast and colon cancersPDCD11SKP2ubiquitination

Identifiers

PMID40051297
PMCPMC12061330

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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.