Evidence map›Paper›PMID 32370197›Full record

ArticleInternational journal of molecular sciences2020

Highly Expressed FOXF1 Inhibit Non-Small-Cell Lung Cancer Growth via Inducing Tumor Suppressor and G1-Phase Cell-Cycle Arrest.

Chia-Yu Wu, Chun-Hao Chan, Navneet Kumar Dubey, Hong-Jian Wei, Jui-Hua Lu, Chun-Chao Chang, Hsin-Chung Cheng, Keng-Liang Ou, Win-Ping Deng

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  10. Decreased HLF Expression Predicts Poor Survival in Lung Adenocarcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2021
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  11. Review
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

9 authors at 4 institutions in 1 country.

Chia-Yu WuDivision of Oral and Maxillofacial Surgery, Department of Dentistry, Taipei Medical University Hospital, Taipei 11031, Taiwan.
Chun-Hao ChanSchool of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei 11031, Taiwan.
Navneet Kumar DubeySchool of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei 11031, Taiwan.
Hong-Jian WeiSchool of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei 11031, Taiwan.
Jui-Hua LuSchool of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei 11031, Taiwan.
Chun-Chao ChangDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Taipei Medical University Hospital, Taipei 11031, Taiwan.
Hsin-Chung ChengSchool of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei 11031, Taiwan.
Keng-Liang OuDepartment of Dentistry, Taipei Medical University-Shuang Ho Hospital, New Taipei City, Taiwan.
Win-Ping DengSchool of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei 11031, Taiwan.
Taipei Medical University · TWTaipei Medical University Hospital · TWFu Jen Catholic University · TWTaipei Medical University-Shuang Ho Hospital · TW

Funding

Ministry of Science and Technology, Taiwan (MOST 104-2313-B-038-001, 104-2221-E-038-016, 105-2314-B-038-011 and 106-2314-B-038-077-MY2)
6 · The paper itself

Abstract

Cancer pathogenesis results from genetic alteration-induced high or low transcriptional programs, which become highly dependent on regulators of gene expression. However, their role in progressive regulation of non-small-cell lung cancer (NSCLC) and how these dependencies may offer opportunities for novel therapeutic options remain to be understood. Previously, we identified forkhead box F1 (FOXF1) as a reprogramming mediator which leads to stemnesss when mesenchymal stem cells fuse with lung cancer cells, and we now examine its effect on lung cancer through establishing lowly and highly expressing FOXF1 NSCLC engineered cell lines. Higher expression of FOXF1 was enabled in cell lines through lentiviral transduction, and their viability, proliferation, and anchorage-dependent growth was assessed. Flow cytometry and Western blot were used to analyze cellular percentage in cell-cycle phases and levels of cellular cyclins, respectively. In mice, tumorigenic behavior of FOXF1 was investigated. We found that FOXF1 was downregulated in lung cancer tissues and cancer cell lines. Cell proliferation and ability of migration, anchorage-independent growth, and transformation were inhibited in H441-FOXF1

Indexed as

Gene Expression Regulation, NeoplasticAnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p21Forkhead Transcription FactorsG1 Phase Cell Cycle CheckpointsHumansLung NeoplasmsMice, Inbred NODMice, SCIDTumor BurdenTumor Suppressor ProteinsXenograft Model Antitumor AssaysCyclin-Dependent Kinase Inhibitor p21Forkhead Transcription FactorsFOXF1 protein, humanTumor Suppressor Proteinscell cyclecell migration, tumor suppressorFOXF1lung cancer

Identifiers

PMID32370197
PMCPMC7246752
OpenAlexW3022394290

What OpenQuestion holds

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LicenceCC BY
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.