Evidence map›Paper›PMID 25356753›Full record

ArticleOncotarget2014

Involvement of FoxQ1 in NSCLC through regulating EMT and increasing chemosensitivity.

Jian Feng, Liqin Xu, Songshi Ni, Jun Gu, Huijun Zhu, Haiying Wang, Shu Zhang, Wei Zhang, Jianfei Huang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. The transcription factor FOXQ1 in cancer.Cancer metastasis reviews · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. The Dominant Role of Forkhead Box Proteins in Cancer.International journal of molecular sciences · 2018
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 2 institutions in 1 country.

Jian FengDepartment of Respiratory Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Liqin XuDepartment of Respiratory Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Songshi NiDepartment of Respiratory Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Jun GuDepartment of Respiratory Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Huijun ZhuDepartment of Pathology, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Haiying WangDepartment of Respiratory Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Shu ZhangDepartment of Pathology, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Wei ZhangDepartment of Pathology, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Jianfei HuangDepartment of Pathology, Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
Nantong University · CNAffiliated Hospital of Nantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Forkhead box Q1 (FoxQ1) is a member of the forkhead transcription factor family. High expression of FoxQ1 has been associated with several cancers including non-small cell lung cancer (NSCLC), but its role in the development of NSCLC is not clear. In this study, we investigated the effect of FoxQ1 up-regulated and down-regulated in vitro and in vivo, and the role of FoxQ1 in regulating epithelial-mesenchymal transition (EMT) in NSCLC, providing evidence that FoxQ1 could be a potential therapeutic target in NSCLC. NSCLC cells with silenced FoxQ1 had decreased cell proliferation, migration and invasion in cell culture and delayed growth of xenograft tumors in mice compared with corresponding control cells. The NSCLC cells downregulated for FoxQ1 induced the expression of apoptosis-associated proteins and reduction of anti-apoptotic protein expression. Downregulation of FoxQ1 promoted the expression of epithelial markers and decreased several mesenchymal markers in vitro and in vivo. In addition, FoxQ1 was associated with resistance to conventional chemotherapeutic agents. In contrast, FoxQ1 overexpressed elicited converse effects on these phenotypes in vitro and in vivo. Our findings define a key role for FoxQ1 in regulating EMT and increasing chemosensitivity in NSCLC.

Indexed as

AnimalsApoptosisCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationCisplatinDeoxycytidineDocetaxelDown-RegulationDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionForkhead Transcription FactorsGemcitabineGene Expression Regulation, NeoplasticGene SilencingCisplatinDeoxycytidineDocetaxelForkhead Transcription FactorsFOXQ1 protein, humanGemcitabineGlutamatesGuaninePemetrexedRNA, MessengerTaxoids

Identifiers

PMID25356753
PMCPMC4259430
OpenAlexW1565758447

What OpenQuestion holds

Textmetadata
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.