Evidence map›Paper›PMID 41413015›Full record

ArticleCell death & disease2025

IFIT3 promotes lymph node metastasis by interacting with LASP1 to activate FAK-ERK signaling in esophageal squamous cell carcinoma.

Qixiao Cui, Xiaolin Zhou, Xiaojie Chen, Xiaochuan Zhao, Rui Zhang, Jince Wang, Xiaoli Li, Guoli Wang, Bohan Li, Minjing Li and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Qixiao Cui *Featured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, Shandong, PR China.
Xiaolin Zhou *Featured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, Shandong, PR China.
Xiaojie Chen *Featured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, Shandong, PR China.
Xiaochuan ZhaoFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, Shandong, PR China.
Rui ZhangFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, Shandong, PR China.
Jince WangFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, Shandong, PR China.
Xiaoli LiFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, Shandong, PR China.
Guoli WangFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, Shandong, PR China.
Bohan LiFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, Shandong, PR China.
Minjing LiFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, Shandong, PR China.ORCID http://orcid.org/0000-0001-9276-4654
Jiajia ChenFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, Shandong, PR China.
Xihang GaoFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, Shandong, PR China.
Yanbing ShiFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, Shandong, PR China.
Wenting LiFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, Shandong, PR China.
Pan HongFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, Shandong, PR China. jcinta_pan@163.com.ORCID http://orcid.org/0000-0001-7262-278X
Defang LiFeatured Laboratory for Biosynthesis and Target Discovery of Active Components of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Binzhou Medical University, Yantai, Shandong, PR China. lidefang@163.com.ORCID http://orcid.org/0000-0003-4151-9151

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82073313National Natural Science Foundation of China (National Science Foundation of China) 82104226
6 · The paper itself

Abstract

Lymph node metastasis (LNM) is an important cause of poor prognosis in patients with esophageal squamous cell carcinoma (ESCC). However, the mechanism of LNM in ESCC has not been elucidated. Here, we identified interferon-induced proteins with tetratricopeptide repeats 3 (IFIT3) highly expressed in ESCC, especially in LNM tissues. IFIT3 overexpression promoted ESCC cell metastasis in vitro and in vivo. Mechanistically, IFIT3 interacted with LIM and SH3 protein 1 (LASP1) and facilitated the localization of LASP1 to the cell edge, promoting the interaction between LASP1 and Talin1 and the binding of Talin1 to integrin, ultimately activating the FAK-ERK signaling pathway. Clinically, IFIT3 and LASP1 were upregulated in ESCC and LNM tissues and associated with poor prognosis. Moreover, patients with high expression of both IFIT3 and LASP1 have a poorer prognosis. In conclusion, IFIT3 promotes LNM in ESCC through the LASP1/FAK/ERK axis, and IFIT3 is a potential therapeutic target for LNM in ESCC.

Indexed as

Adaptor Proteins, Signal TransducingCytoskeletal ProteinsEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaFocal Adhesion Kinase 1Intracellular Signaling Peptides and ProteinsLIM Domain ProteinsMAP Kinase Signaling SystemAnimalsCell Line, TumorCell MovementFemaleGene Expression Regulation, NeoplasticHumansLymphatic MetastasisMaleAdaptor Proteins, Signal TransducingCytoskeletal ProteinsFocal Adhesion Kinase 1Intracellular Signaling Peptides and ProteinsLASP1 protein, humanLIM Domain ProteinsPTK2 protein, human

Identifiers

PMID41413015
PMCPMC12847741

What Socratic holds

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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.