Evidence map›Paper›PMID 40567051›Full record

ArticleActa biochimica et biophysica Sinica2025

Therapeutic potential of targeting the NEDD4L-eEF1A1 axis in cancer therapy.

Yan Qin, Xinyue Wang, Minghui Zhao, Yuehui Liu, Huiyi Hou, Tingting Wang, Yuhe Pei, Jingxin Zhang, Zhou Shen, Feixiang Wu and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2025. 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

14 authors.

Yan QinCentral Laboratory, Affiliated Hospital of Hebei University, Baoding 071000, China.
Xinyue WangClinical Medical College, Hebei University, Baoding 071000, China.
Minghui ZhaoHebei Key Laboratory of Precise Imaging of Inflammation Related Tumors, Baoding 071000, China.
Yuehui LiuClinical Medical College, Hebei Medical University, Shijiazhuang 050000, China.
Huiyi HouClinical Medical College, Hebei University, Baoding 071000, China.
Tingting WangClinical Medical College, Hebei University, Baoding 071000, China.
Yuhe PeiClinical Medical College, Hebei University, Baoding 071000, China.
Jingxin ZhangClinical Medical College, Hebei University, Baoding 071000, China.
Zhou ShenCentral Laboratory, Affiliated Hospital of Hebei University, Baoding 071000, China.
Feixiang WuCentral Laboratory, Affiliated Hospital of Hebei University, Baoding 071000, China.
Lishuang ZhengCentral Laboratory, Affiliated Hospital of Hebei University, Baoding 071000, China.
Jinghua LiHepatobiliary Surgery, Affiliated Hospital of Hebei University, Baoding 071000 China.
Zhiyu NiHebei Collaborative Innovation Center of Tumor Microecological Metabolism Regulation, Baoding 071000, China.
Jianhong ShiCentral Laboratory, Affiliated Hospital of Hebei University, Baoding 071000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abnormal proliferation and migration of endothelial cells are key contributors to tumor angiogenesis. Recent studies have shown that the crucial role of E3 ubiquitin ligase neuronal precursor cell expression developmentally downregulated 4-like (NEDD4L) in tumorigenesis. However, the precise mechanisms by which NEDD4L functions in endothelial cells remain unclear. In this study, we investigate the mechanisms by which NEDD4L influences the function of human umbilical vein endothelial cells (HUVECs) and its effect on tumor angiogenesis. Our results show that NEDD4L overexpression in HUVECs suppresses both cell proliferation and migration. Additionally, we find that the autophagic activity in NEDD4L-overexpressing cells is increased. Proteomic profiling and ubiquitination assays reveal that NEDD4L interacts with eEF1A1, promoting K48-linked ubiquitination-mediated degradation of eEF1A1. This post-translational modification is a key step in the NEDD4L-mediated regulation of autophagy and cellular function. Moreover, we find that loss of endothelial NEDD4L significantly enhances tumor growth and promotes angiogenesis

Indexed as

Nedd4 Ubiquitin Protein LigasesNeoplasmsPeptide Elongation Factor 1AnimalsAutophagyCell MovementCell ProliferationHumansHuman Umbilical Vein Endothelial CellsMiceMice, NudeNeovascularization, PathologicUbiquitinationEEF1A1 protein, humanNedd4L protein, humanNedd4 Ubiquitin Protein LigasesPeptide Elongation Factor 1angiogenesisautophagyeEF1A1migrationNEDD4Lproliferationubiquitination

Identifiers

PMID40567051
PMCPMC12900694

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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.