Evidence map›Paper›PMID 41559059›Full record

ArticleNature communications2026

Targeting the UFL1-AKT cascade suppresses triple-negative breast cancer progression.

Xiao Yang, Yalei Wen, Xiuqing Ma, Shengying Qin, Yixia Liu, Jiaqi Chen, Haoxing Zhang, Colin R Goding, Rutao Cui, Tongzheng Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

10 authors.

Xiao Yang *Department of General Surgery, Guangzhou Red Cross Hospital of Jinan University, Guangzhou, China.
Yalei Wen *College of Pharmacy, Jinan University, Guangzhou, China.
Xiuqing Ma *College of Pharmacy, Jinan University, Guangzhou, China.
Shengying Qin *Department of Oncology, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Yixia LiuCollege of Pharmacy, Jinan University, Guangzhou, China.
Jiaqi ChenCollege of Pharmacy, Jinan University, Guangzhou, China.
Haoxing ZhangGuangdong Provincial Key Laboratory of Genome Stability and Disease Prevention, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen, China.ORCID http://orcid.org/0000-0002-0551-2916
Colin R GodingLudwig Institute for Cancer Research, University of Oxford, Headington, Oxford, UK.ORCID http://orcid.org/0000-0002-1614-3909
Rutao CuiZhejiang University School of Medicine, Hangzhou, China.ORCID http://orcid.org/0009-0004-2590-0475
Tongzheng LiuDepartment of General Surgery, Guangzhou Red Cross Hospital of Jinan University, Guangzhou, China. liutongzheng@jnu.edu.cn.ORCID http://orcid.org/0000-0003-0859-3923

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82404654National Natural Science Foundation of China (National Science Foundation of China) 82473109
6 · The paper itself

Abstract

Triple-negative breast cancer (TNBC) is an aggressive and highly lethal disease with limited therapies. While UFL1-mediated UFMylation has been implicated in various diseases, its role in TNBC remains not fully understood. Here, we demonstrate that AKT1 directly interacts with UFL1 and undergoes UFMylation at Lys189/276/297. This modification enhances AKT phosphorylation and activation, promoting tumor growth and chemoresistance in TNBC. In turn, AKT phosphorylates UFL1 at Thr426, establishing a positive feedback loop that sustains high activity of both pro-oncogenic regulators in TNBC. Disrupting the UFL1-AKT interaction using the specific peptide PDAU-TAT significantly inhibits TNBC progression both in vitro and in vivo. Clinically, elevated pT426 UFL1 correlates with high pAKT in TNBC specimens. These findings uncover a crucial UFL1-AKT positive feedback loop that drives TNBC progression and suggest that targeting this axis could offer a promising therapeutic strategy for TNBC and potentially other aggressive cancers characterized by upregulated UFL1 and AKT activation.

Indexed as

Proto-Oncogene Proteins c-aktTriple Negative Breast NeoplasmsAnimalsCell Line, TumorCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMicePhosphorylationSignal TransductionAKT1 protein, humanProto-Oncogene Proteins c-akt

Identifiers

PMID41559059
PMCPMC12820175

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.