Evidence map›Paper›PMID 36924014›Full record

ArticleThoracic cancer2023

MARVELD3 inhibits the epithelial-mesenchymal transition and cell migration by suppressing the Wnt/β-catenin signaling pathway in non-small cell lung cancer cells.

Shirong Li, Saiping Qi, Yanmeng Li, Chunpan Zhang, Lan Sun, Chunquan Liu, Haoyan Wang

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.2field-weighted citation impact, top 13% of its field
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

8 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.International journal of biological sciences · 2025
    Review
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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

7 authors at 1 institution in 1 country.

Shirong LiDepartment of Infectious Disease, Beijing Friendship Hospital, Capital Medical University, Beijing, China.ORCID 0000-0003-0227-901X
Saiping QiBeijing Institute of Clinical medicine Research, Beijing Friendship Hospital, Capital Medical University, Beijing, China.ORCID 0000-0002-8168-842X
Yanmeng LiBeijing Institute of Clinical medicine Research, Beijing Friendship Hospital, Capital Medical University, Beijing, China.ORCID 0000-0003-3151-7099
Chunpan ZhangBeijing Institute of Clinical medicine Research, Beijing Friendship Hospital, Capital Medical University, Beijing, China.ORCID 0000-0002-4750-2564
Lan SunDepartment of Pathology, Beijing Friendship Hospital, Capital Medical University, Beijing, China.ORCID 0000-0003-2623-9645
Chunquan LiuDepartment of Thoracic Surgery, Beijing Friendship Hospital, Capital Medical University, Beijing, China.ORCID 0000-0002-7075-3732
Haoyan WangDepartment of Respiratory Medicine, Beijing Friendship Hospital, Capital Medical University, Beijing, China.ORCID 0000-0002-2534-3590
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe epithelial-mesenchymal transition (EMT), featured by abatement of cell-cell contact, is related to exacerbating non-small cell lung cancer (NSCLC) by inducing metastasis. MAL and relevant proteins for vesicle trafficking and membrane link domain 3 (MARVELD3) is a novel tight junction protein participated in the EMT. There is limited information available about the mechanism of MARVELD3 in NSCLC. In this trial, the inhibition effect of MARVELD3 on human NSCLC cells will be discussed.

methodsMARVELD3 expression was measured in NSCLC tissues and para-carcinoma tissues. The expression of MARVELD3 and EMT-related genes were examined in transforming growth factor (TGF)-β1-induced NSCLC cells. NSCLC cells with MARVELD3-knockdown and overexpressed were established to analyze the relationship between MARVELD3 and EMT and cell migration. The Wnt/β-catenin pathway expression was also analyzed in NSCLC cell models and clinic species.

resultsLower protein levels of MARVELD3 were observed in NSCLC samples than para-carcinoma specimens, and the decreased expression of MARVELD3 in NSCLC specimens was associated with tumor metastasis. E-Cadherin and MARVELD3 expression was reduced in TGF-β1 treated NSCLC cells, whereas increased Vimentin expression was detected. MARVELD3 changed the EMT-related genes and induced cell migration. In addition, Wnt/β-catenin pathway and target genes, MYC and CCND1, expressions were inhibited in MARVELD3 overexpressed NSCLC cells.

conclusionsTGF-β1 induced EMT in human NSCLC cells can be suppressed by MARVELD3 through Wnt/β-catenin signaling pathway. These results indicate that MARVELD3 might be a potential therapeutic modality useful in the treatment of NSCLC.

Indexed as

CarcinomaCarcinoma, Non-Small-Cell LungLung Neoplasmsbeta CateninCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionHumansMembrane ProteinsTransforming Growth Factor beta1Wnt Signaling Pathwaybeta CateninMARVELD3 protein, humanMembrane ProteinsTransforming Growth Factor beta1EMTMARVELD3NSCLCTGF-β1Wnt/β-catenin

Identifiers

PMID36924014
PMCPMC10125787
OpenAlexW4327682137

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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 OpenQuestion graph.