Evidence map›Paper›PMID 31060551›Full record

ArticleJournal of translational medicine2019

SOX9 drives the epithelial-mesenchymal transition in non-small-cell lung cancer through the Wnt/β-catenin pathway.

Jing-Qiang Huang, Fa-Kai Wei, Xiu-Li Xu, Shi-Xing Ye, Jun-Wei Song, Pei-Kun Ding, Jing Zhu, He-Feng Li, Xin-Ping Luo, Hui Gong and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

76 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.

  1. Pooled it
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  9. Frontiers in cell and developmental biology · 2025
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  13. Tankyrase 2 promotes lung cancer cell malignancy.World journal of clinical oncology · 2024
    Article
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16 more citing papers are in PubMed but not listed here.

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

13 authors at 3 institutions in 1 country.

Jing-Qiang HuangGuangdong Key Laboratory for Genome Stability and Human Disease Prevention, Department of Biochemistry and Molecular Biology, Health Science Center, Shenzhen University, Shenzhen, 518060, People's Republic of China.
Fa-Kai WeiGuangdong Key Laboratory for Genome Stability and Human Disease Prevention, Department of Biochemistry and Molecular Biology, Health Science Center, Shenzhen University, Shenzhen, 518060, People's Republic of China.
Xiu-Li XuGuangdong Key Laboratory for Genome Stability and Human Disease Prevention, Department of Biochemistry and Molecular Biology, Health Science Center, Shenzhen University, Shenzhen, 518060, People's Republic of China.
Shi-Xing YeDepartment of Equipment, Shenzhen Longhua People's Hospital, Shenzhen, 518109, People's Republic of China.
Jun-Wei SongGuangdong Key Laboratory for Genome Stability and Human Disease Prevention, Department of Biochemistry and Molecular Biology, Health Science Center, Shenzhen University, Shenzhen, 518060, People's Republic of China.
Pei-Kun DingDepartment of Thoracic Surgery, Shenzhen People's Hospital, 2nd Clinical Medical College of Jinan University, Shenzhen, 518020, People's Republic of China.
Jing ZhuGuangdong Key Laboratory for Genome Stability and Human Disease Prevention, Department of Biochemistry and Molecular Biology, Health Science Center, Shenzhen University, Shenzhen, 518060, People's Republic of China.
He-Feng LiGuangdong Key Laboratory for Genome Stability and Human Disease Prevention, Department of Biochemistry and Molecular Biology, Health Science Center, Shenzhen University, Shenzhen, 518060, People's Republic of China.
Xin-Ping LuoGuangdong Key Laboratory for Genome Stability and Human Disease Prevention, Department of Biochemistry and Molecular Biology, Health Science Center, Shenzhen University, Shenzhen, 518060, People's Republic of China.
Hui GongCentral Laboratory, Shenzhen Nanshan People's Hospital, Shenzhen University, Shenzhen, 518052, People's Republic of China.
Li SuKey Laboratory of Molecular Biophysics of Ministry of Education, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, 430074, China.
Lin YangDepartment of Thoracic Surgery, Shenzhen People's Hospital, 2nd Clinical Medical College of Jinan University, Shenzhen, 518020, People's Republic of China. 13798314779@163.com.
Li-Yun GongGuangdong Key Laboratory for Genome Stability and Human Disease Prevention, Department of Biochemistry and Molecular Biology, Health Science Center, Shenzhen University, Shenzhen, 518060, People's Republic of China. gongly@szu.edu.cn.
Shenzhen University Health Science Center · CNShenZhen People’s Hospital · CNShenzhen Institute of Information Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe distant metastasis of cancer cells is a risk factor for tumor lethality and poor prognosis in non-small-cell lung carcinoma (NSCLC). Increased SOX9 expression has been associated with clinical stage and poor prognosis in NSCLC, but the molecular mechanisms by which SOX9 promotes metastasis in NSCLC are still unknown.

methodsThe relationship between SOX9 expression and T, N, M classification was assessed using the χ

resultsWe found that SOX9 overexpression correlates with the T, N and M stage significantly (p = 0.03, 0.000, and 0.032 respectively) in 142 immunohistochemically diagnosed specimens of NSCLC. SOX9 overexpression was found to decrease the expression of the epithelial cell markers E-cadherin and γ-catenin and increase the expression of the mesenchymal cell markers N-cadherin and vimentin. An in vivo assay showed distant metastasis of the SOX9-overexpressing cells, which was not observed in the SOX9-knockdown cells. These findings indicate that SOX9 promotes distant metastasis by promoting EMT in NSCLC cells. GSEA showed that SOX9 overexpression was significantly correlated with the Wnt/β-catenin pathway which was corroborated by the expression of EMT-associated proteins in this pathway and its downstream target genes. SOX9 overexpression was also found to enhance the transcriptional activity of TCF/LEF, promote the nuclear translocation of β-catenin and increase the phosphorylation of GSK3β at Ser9. Further, inhibition of β-catenin suppressed the metastasis-promoting effects of SOX9 overexpression.

conclusionsThis study is the first to report that SOX9 is associated with clinical TNM stage and indicates that SOX9 promotes migration, invasion and the EMT process through the Wnt/β-catenin pathway.

Indexed as

Epithelial-Mesenchymal TransitionWnt Signaling PathwayAnimalsbeta CateninCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell NucleusHeterocyclic Compounds, 3-RingHumansLung NeoplasmsNeoplasm InvasivenessNeoplasm MetastasisNeoplasm StagingSOX9 Transcription FactorZebrafishbeta CateninHeterocyclic Compounds, 3-RingSOX9 protein, humanSOX9 Transcription FactorXAV939EMTMetastasisNSCLCSOX9Wnt/β-catenin

Identifiers

PMID31060551
PMCPMC6501400
OpenAlexW2945527196

What OpenQuestion holds

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LicenceCC BY
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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.