Evidence map›Paper›PMID 37718450›Full record

ArticleJournal of translational medicine2023

LAD1 promotes malignant progression by diminishing ubiquitin-dependent degradation of vimentin in gastric cancer.

Yingming Jiang, Yanchun Feng, Jintuan Huang, Zhenze Huang, Rongchang Tan, Tuoyang Li, Zijian Chen, Xiaocheng Tang, Jun Qiu, Chujun Li and 2 more

Abstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

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  6. Identification of potential biomarkers for hypertension based on transcriptomic analysis in rats.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
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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

12 authors.

Yingming Jiang *Department of Gastrointestinal Endoscopy, Department of General Surgery, The Sixth Affiliated Hospital, Sun Yat-Sen University, 510655, Guangzhou, China.
Yanchun Feng *Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Diseases, The Sixth Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510655, China.
Jintuan Huang *Department of Gastric Surgery Section 2, Department of General Surgery, The Sixth Affiliated Hospital, Sun Yat-Sen University, 510655, Guangzhou, China.
Zhenze Huang *Department of Gastric Surgery Section 2, Department of General Surgery, The Sixth Affiliated Hospital, Sun Yat-Sen University, 510655, Guangzhou, China.
Rongchang TanDepartment of Gastric Surgery Section 2, Department of General Surgery, The Sixth Affiliated Hospital, Sun Yat-Sen University, 510655, Guangzhou, China.
Tuoyang LiDepartment of Gastric Surgery Section 2, Department of General Surgery, The Sixth Affiliated Hospital, Sun Yat-Sen University, 510655, Guangzhou, China.
Zijian ChenDepartment of Gastric Surgery Section 2, Department of General Surgery, The Sixth Affiliated Hospital, Sun Yat-Sen University, 510655, Guangzhou, China.
Xiaocheng TangDepartment of Gastric Surgery Section 2, Department of General Surgery, The Sixth Affiliated Hospital, Sun Yat-Sen University, 510655, Guangzhou, China.
Jun QiuDepartment of Gastric Surgery Section 2, Department of General Surgery, The Sixth Affiliated Hospital, Sun Yat-Sen University, 510655, Guangzhou, China.
Chujun LiDepartment of Gastrointestinal Endoscopy, Department of General Surgery, The Sixth Affiliated Hospital, Sun Yat-Sen University, 510655, Guangzhou, China. lichujun@mail.sysu.edu.cn.
Hao ChenDepartment of Gastric Surgery Section 2, Department of General Surgery, The Sixth Affiliated Hospital, Sun Yat-Sen University, 510655, Guangzhou, China. chenhao29@mail.sysu.edu.cn.
Zuli YangDepartment of Gastric Surgery Section 2, Department of General Surgery, The Sixth Affiliated Hospital, Sun Yat-Sen University, 510655, Guangzhou, China. yangzuli@mail.sysu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLadinin-1 (LAD1), an anchoring filament protein, has been associated with several cancer types, including cancers of the colon, lungs, and breast. However, it is still unclear how and why LAD1 causes gastric cancer (GC).

methodsMultiple in vitro and in vivo, functional gains and loss experiments were carried out in the current study to confirm the function of LAD1. Mass spectrometry was used to find the proteins that interact with LAD1. Immunoprecipitation analyses revealed the mechanism of LAD1 involved in promoting aggressiveness.

resultsThe results revealed that the LAD1 was overexpressed in GC tissues, and participants with increased LAD1 expression exhibited poorer disease-free survival (DFS) and overall survival (OS). Functionally, LAD1 promotes cellular invasion, migration, proliferation, and chemoresistance in vivo and in vitro in the subcutaneous patient-and cell-derived xenograft (PDX and CDX) tumor models. Mechanistically, LAD1 competitively bound to Vimentin, preventing it from interacting with the E3 ubiquitin ligase macrophage erythroblast attacher (MAEA), which led to a reduction in K48-linked ubiquitination of Vimentin and an increase in Vimentin protein levels in GC cells.

conclusionsIn conclusion, the current investigation indicated that LAD1 has been predicted as a possible prognostic biomarker and therapeutic target for GC due to its ability to suppress Vimentin-MAEA interaction.

Indexed as

Stomach NeoplasmsAnimalsBreastDisease Models, AnimalHumansUbiquitinUbiquitinationVimentinUbiquitinVimentinGastric cancerLAD1MAEAUbiquitinationVimentin

Identifiers

PMID37718450
PMCPMC10506284

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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.