Evidence map›Paper›PMID 30221666›Full record

ArticleMolecular medicine reports2018

Downregulation of FOXK2 is associated with poor prognosis in patients with gastric cancer.

Xi Liu, Xiaodong Wei, Wei Niu, Dong Wang, Bo Wang, Hao Zhuang

Abstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. AKT Phosphorylation of FOXK2 at Ser398 Impacts Breast Cancer Cell Growth and Viability.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Review
  3. Genes & diseases · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. The deacetylation of Foxk2 by Sirt1 reduces chemosensitivity to cisplatin.Journal of cellular and molecular medicine · 2022
    Article
  8. Review
  9. Regulation and roles of FOXK2 in cancer.Frontiers in oncology · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. 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

6 authors.

Xi LiuDepartment of Gastroenterology, Tianjin Nankai Hospital, Tianjin 300100, P.R. China.
Xiaodong WeiDepartment of Gastroenterology, Tianjin Nankai Hospital, Tianjin 300100, P.R. China.
Wei NiuDepartment of Gastroenterology, Tianjin Nankai Hospital, Tianjin 300100, P.R. China.
Dong WangDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Bo WangDepartment of Neurosurgery, Tianjin Huanhu Hospital, Tianjin 300050, P.R. China.
Hao ZhuangDepartment of Hepatic Biliary Pancreatic Surgery, Cancer Hospital Affiliated to Zhengzhou University, Zhengzhou, Henan 450008, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Forkhead box (FOX)K2 (FOXK2) is a member of the FOX transcription factor family. It has been suggested previously that FOXK2 is required to suppress tumor growth; however, the exact role of FOXK2 in gastric cancer remains to be elucidated. In the present study, the association between FOXK2 expression and the clinicopathological characteristics of patients with gastric cancer was investigated. The prognostic value of FOXK2 expression and the significance of clinicopathological parameters in the overall survival (OS) and progression‑free survival of patients were also determined by survival analysis. To investigate the functional roles of FOXK2, it was downregulated in BGC‑823 cells using small interfering (si)RNA, and upregulated using a FOXK2 plasmid. Colony formation, Cell Counting Kit‑8 and cell proliferation analyses were conducted to examine the proliferation of gastric cancer cells. Transwell and wound‑healing assays were performed to investigate the effect of FOXK2 expression on gastric cancer cell migration and invasion. The clinical data demonstrated that FOXK2 expression was reduced in high‑grade gastric cancer tissues, and a low level of FOXK2 expression indicated a poor prognosis. The data obtained from the Human Protein Atlas revealed that patients with gastric cancer and a high level of FOXK2 expression had a longer OS time. The results of colony formation assays, Transwell and wound healing assays demonstrated that FOXK2 repressed the proliferation, invasion and migration of gastric cancer cells, respectively. The findings indicated that FOXK2 may serve as a promising therapeutic target in gastric cancer. Taken together, the findings of the present study demonstrated that FOXK2 functions as a tumor suppressor in gastric cancer; the loss of FOXK2 may induce the growth and invasion of gastric cancer cells.

Indexed as

PrognosisAdultAgedCell Line, TumorCell MovementCell ProliferationDisease-Free SurvivalFemaleForkhead Transcription FactorsGene Expression Regulation, NeoplasticHumansMaleMiddle AgedNeoplasm InvasivenessStomach NeoplasmsForkhead Transcription Factorsinterleukin binding factor

Identifiers

PMID30221666
PMCPMC6172389

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Registered trials

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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.