Evidence map›Paper›PMID 30094882›Full record

ArticleCell proliferation2018

FBXW7 suppresses epithelial-mesenchymal transition and chemo-resistance of non-small-cell lung cancer cells by targeting snai1 for ubiquitin-dependent degradation.

Guodong Xiao, Yuan Li, Meng Wang, Xiang Li, Sida Qin, Xin Sun, Rui Liang, Boxiang Zhang, Ning Du, Chongwen Xu and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell proliferation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

45 citing papers in PubMed, 77 citations in OpenAlex.

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  7. Role of Ubiquitin-regulated EMT in Cancer Metastasis and Chemoresistance.International journal of biological sciences · 2025
    Review
  8. Molecular insights and clinical implications for the tumor suppressor role of SCFBiochimica et biophysica acta. Reviews on cancer · 2024
    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

12 authors at 3 institutions in 1 country.

Guodong XiaoDepartment of Thoracic Surgery and Oncology, The Second Department of Thoracic Surgery, Cancer Center, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.ORCID http://orcid.org/0000-0002-8739-5513
Yuan LiSchool of Humanities & Social Sciences, Xi'an Jiaotong University, Xi'an, China.
Meng WangDepartment of Thoracic Surgery and Oncology, The Second Department of Thoracic Surgery, Cancer Center, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Xiang LiDepartment of Thoracic Surgery and Oncology, The Second Department of Thoracic Surgery, Cancer Center, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Sida QinDepartment of Thoracic Surgery and Oncology, The Second Department of Thoracic Surgery, Cancer Center, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Xin SunDepartment of Thoracic Surgery and Oncology, The Second Department of Thoracic Surgery, Cancer Center, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Rui LiangDepartment of Hepatobiliary Chest Surgery, Shaanxi Provincial Corps Hospital of Chinese People's Armed Police Force, Xi'an, China.
Boxiang ZhangDepartment of Thoracic Surgery and Oncology, The Second Department of Thoracic Surgery, Cancer Center, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Ning DuDepartment of Thoracic Surgery and Oncology, The Second Department of Thoracic Surgery, Cancer Center, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Chongwen XuDepartment of Otorhinolaryngology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Hong RenDepartment of Thoracic Surgery and Oncology, The Second Department of Thoracic Surgery, Cancer Center, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Dapeng LiuDepartment of Thoracic Surgery and Oncology, The Second Department of Thoracic Surgery, Cancer Center, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
First Affiliated Hospital of Xi'an Jiaotong University · CNJiangSu Armed Police General Hospital · CNXi'an Jiaotong University · CN

Funding

Key Research and Development Program of Shaanxi Province 2017KW-061National Natural Science Foundation of China 81272418National Natural Science Foundation of China 81602597
6 · The paper itself

Abstract

objectivesFBXW7 acts as a tumour suppressor by targeting at various oncoproteins for ubiquitin-mediated degradation. However, the clinical significance and the involving regulatory mechanisms of FBXW7 manipulation of NSCLC regeneration and therapy response are not clear. MATERIALS AND

methodsImmunohistochemical staining and qRT-PCR were applied to detect FBXW7 and Snai1 expression in 100 samples of NSCLC and matched tumour-adjacent tissues. FBXW7 manipulation of cancer biological functions were studied by using MTT assay, immunoblotting, flow cytometry, transwells, wound healing assay, and sphere-formation assays. Immunofluorescence and co-immunoprecipitation were used to analyse the possible interaction between Snai1 and FBXW7.

resultsWe detected the decreased FBXW7 expression in majority of the NSCLC tissues, and lower FBXW7 level was correlated with advanced TNM stage. Furthermore, those patients with decreased FBXW7 expression tend to have both poorer 5-year survival outcomes, and shorter disease-free survival, comparing to those with higher FBXW7 levels. Functionally, we found that FBXW7 enforcement suppressed NSCLC progression by inducing cell growth arrest, increasing chemo-sensitivity and inhibiting Epithelial-mesenchymal Transition (EMT) progress. Results further showed that FBXW7 could interact with Snai1 directly to degrade its expression through ubiquitylating alternation in NSCLC, which could be partially abrogated by restoring Snai1 expression.

conclusionsFBXW7 conduction of tumour suppression was partly through degrading Snai1 directly for ubiquitylating regulation in NSCLC.

Indexed as

A549 CellsCarcinoma, Non-Small-Cell LungCell Cycle ProteinsCell Line, TumorCell ProliferationDisease-Free SurvivalDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionF-Box-WD Repeat-Containing Protein 7FemaleHEK293 CellsHumansLung NeoplasmsMaleMiddle AgedSnail Family Transcription FactorsCell Cycle ProteinsF-Box-WD Repeat-Containing Protein 7FBXW7 protein, humanSNAI1 protein, humanSnail Family Transcription FactorsUbiquitincancer stem-like cellschemotherapy resistanceepithelial-mesenchymal transitionFBXW7non-small-cell lung cancersnai1

Identifiers

PMID30094882
PMCPMC6528938
OpenAlexW2887485171

What OpenQuestion holds

Textmetadata
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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.