Evidence map›Paper›PMID 25561901›Full record

ArticleInternational journal of biological sciences2015

FOXM1 promotes lung adenocarcinoma invasion and metastasis by upregulating SNAIL.

Ping Wei, Nu Zhang, Yiqin Wang, Dawei Li, Lisha Wang, Xiangjie Sun, Chen Shen, Yusi Yang, Xiaoyan Zhou, Xiang Du

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of biological sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

57 citing papers in PubMed, 77 citations in OpenAlex.

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  14. DOCK2 Promotes Asthma Development by Eliciting Airway Epithelial-Mesenchymal Transition.American journal of respiratory cell and molecular biology · 2023
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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

10 authors at 4 institutions in 1 country.

Ping Wei1. Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, China ; 2. Institute of Pathology, Fudan University, Shanghai 200032, China ; 3. Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, 200032, China ; 6. Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Nu Zhang7. Department of neurosurgery, 1st affiliated hospital of Sun Yat-sen University, Guangzhou, 510080, China.
Yiqin Wang1. Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, China ; 2. Institute of Pathology, Fudan University, Shanghai 200032, China ; 4. Institute of Biomedical Sciences, Fudan University, Shanghai 200032, China. ; 6. Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Dawei Li5. Department of Colorectal Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, China ; 6. Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Lisha Wang1. Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, China ; 2. Institute of Pathology, Fudan University, Shanghai 200032, China ; 4. Institute of Biomedical Sciences, Fudan University, Shanghai 200032, China. ; 6. Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Xiangjie Sun1. Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, China ; 2. Institute of Pathology, Fudan University, Shanghai 200032, China ; 4. Institute of Biomedical Sciences, Fudan University, Shanghai 200032, China. ; 6. Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Chen Shen1. Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, China ; 2. Institute of Pathology, Fudan University, Shanghai 200032, China ; 4. Institute of Biomedical Sciences, Fudan University, Shanghai 200032, China. ; 6. Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Yusi Yang1. Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, China ; 2. Institute of Pathology, Fudan University, Shanghai 200032, China ; 4. Institute of Biomedical Sciences, Fudan University, Shanghai 200032, China. ; 6. Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Xiaoyan Zhou1. Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, China ; 2. Institute of Pathology, Fudan University, Shanghai 200032, China ; 4. Institute of Biomedical Sciences, Fudan University, Shanghai 200032, China. ; 6. Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Xiang Du1. Department of Pathology, Fudan University Shanghai Cancer Center, Shanghai 200032, China ; 2. Institute of Pathology, Fudan University, Shanghai 200032, China ; 4. Institute of Biomedical Sciences, Fudan University, Shanghai 200032, China. ; 6. Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China.
Fudan University Shanghai Cancer Center · CNFudan University · CNShanghai Medical College of Fudan University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The forkhead box M1 (FOXM1) transcription factor is one of the key genes inducing tumor invasion and metastasis by an unknown mechanism. In this study, we set out to investigate the effects of FOXM1 overexpression on metastatic human lung adenocarcinoma and the underlying mechanism. FOXM1 expression was analyzed in 78 frozen lung adenocarcinoma tissue samples using an Affymetrix microarray and a 155-paraffin-embedded lung adenocarcinoma tissue microarray with immunohistochemical detection. FOXM1 was found to be overexpressed in lung adenocarcinoma, particularly in metastatic patients, compared to non-metastatic patients. Knockdown of FOXM1 by a specific siRNA significantly suppressed EMT progression, migration and invasion of lung adenocarcinoma cells in vitro, and tumor growth and metastasis in vivo, whereas restored expression of FOXM1 had the opposite effect. FOXM1 binds directly to the SNAIL promoter through two specific binding sites and constitutively transactivates it. Collectively, our findings indicate that FOXM1 may play an important role in advancing lung adenocarcinoma progression. Aberrant FOXM1 expression directly and constitutively activates SNAIL, thereby promoting lung adenocarcinoma metastasis. Inhibition of FOXM1-SNAIL signaling may present an ideal target for future treatment.

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinomaAdenocarcinoma of LungAnimalsCell Line, TumorCell MovementCell SurvivalForkhead Box Protein M1Forkhead Transcription FactorsHumansLung NeoplasmsMiceNeoplasm InvasivenessSnail Family Transcription FactorsTranscription FactorsForkhead Box Protein M1Forkhead Transcription FactorsFOXM1 protein, humanSnail Family Transcription FactorsTranscription FactorsFOXM1InvasionLung adenocarcinomaMetastasisSNAIL

Identifiers

PMID25561901
PMCPMC4279094
OpenAlexW2163569233

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.