Evidence map›Paper›PMID 31597217›Full record

ArticleCancer science2019

Forkhead box C1 promotes metastasis and invasion of non-small cell lung cancer by binding directly to the lysyl oxidase promoter.

Rumei Gong, Wenli Lin, Aiqin Gao, Yanli Liu, Juan Li, Meili Sun, Xiaozheng Chen, Shuyi Han, Chengsong Men, Yuping Sun and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

18 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  3. Tankyrase 2 promotes lung cancer cell malignancy.World journal of clinical oncology · 2024
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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

11 authors at 2 institutions in 1 country.

Rumei GongDepartment of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.ORCID https://orcid.org/0000-0002-9047-3076
Wenli LinDepartment of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.
Aiqin GaoDepartment of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.
Yanli LiuProvincial Key Laboratory of Radio-Oncology, Shandong Cancer Hospital and Institute, Jinan, China.
Juan LiDepartment of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.
Meili SunDepartment of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.
Xiaozheng ChenDepartment of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.
Shuyi HanGenetic and Molecular Diagnostic Center, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.
Chengsong MenDepartment of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.
Yuping SunDepartment of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.
Jie LiuDepartment of Oncology, Jinan Central Hospital Affiliated to Shandong University, Jinan, China.
Shandong University · CNShandong Tumor Hospital · CN

Funding

Jinan Scientific and Technological Research Fund for Youth 20110321Scientific and Technical Innovation Plan in clinical medicine of Jinan 201805086the National Natural Science Foundation of China 81501989
6 · The paper itself

Abstract

Increasing evidence indicates that human forkhead box C1 (FOXC1) plays important roles in tumor development and metastasis. However, the underlying molecular mechanism of FOXC1 in non-small cell lung cancer (NSCLC) metastasis remains unclear. Here, we identified FOXC1 as an independent prognostic factor in NSCLC and showed clear biological implications in invasion and metastasis. FOXC1 overexpression enhanced the proliferation, migration and invasion of NSCLC cells, whereas FOXC1 silencing impaired the effects both in vitro and in vivo. Importantly, we found a positive correlation between FOXC1 expression and lysyl oxidase (LOX) expression in NSCLC cells and patient samples. Downregulation of LOX or LOX activity inhibition in NSCLC cells inhibited the FOXC1-driven effects on cellular migration and invasion. Xenograft models showed that inhibition of LOX activity by β-aminopropionitrile monofumarate decreased the number of lung metastases. Mechanistically, we demonstrated a novel FOXC1-LOX mechanism that was involved in the invasion and metastasis of NSCLC. Dual-luciferase assay and ChIP identified that FOXC1 bound directly in the LOX promoter region and activated its transcription. Collectively, the present study offered new insight into FOXC1 in the mediation of NSCLC metastasis through interaction with the LOX promoter and further revealed that targeted inhibition of LOX protein activity could prevent lung metastasis in murine xenograft models. These data implicated FOXC1 as a potential therapeutic strategy for the treatment of NSCLC metastasis.

Indexed as

Promoter Regions, GeneticAdultAgedCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationFemaleForkhead Transcription FactorsHumansLung NeoplasmsMaleMiddle AgedNeoplasm InvasivenessPrognosisProtein-Lysine 6-OxidaseForkhead Transcription FactorsFOXC1 protein, humanProtein-Lysine 6-OxidaseFOXC1invasionLOXmetastasisNSCLC

Identifiers

PMID31597217
PMCPMC6890438
OpenAlexW2979766755

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

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.