Evidence map›Paper›PMID 28209947›Full record

ArticleMedical science monitor : international medical journal of experimental and clinical research2017

Forkhead Box Protein J1 (FOXJ1) is Overexpressed in Colorectal Cancer and Promotes Nuclear Translocation of β-Catenin in SW620 Cells.

Kuiliang Liu, Jianghao Fan, Jing Wu

Open access · hybridAbstract read
In one paragraph

Article in Medical science monitor : international medical journal of experimental and clinical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Telomere-Associated Gene Signatures Correlate with Prognosis, Tumor Microenvironment, and Chemosensitivity in Breast Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2023
    Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. 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

3 authors at 2 institutions in 1 country.

Kuiliang LiuDepartment of Gastroenterology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China (mainland).
Jianghao FanDepartment of Gastroenterology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China (mainland).
Jing WuDepartment of Gastroenterology, Beijing Shijitan Hospital, Capital Medical University, Beijing, China (mainland).
Beijing Shijitan Hospital · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND FOXJ1, which is a forkhead transcription factor, has been previously studied mostly as a ciliary transcription factor. The role of FOXJ1 in cancer progression is still elusive and controversial. In the present study, the effect of FOXJ1 in progression of colorectal cancer (CRC) was investigated. MATERIAL AND METHODS The pattern of FOXJ1 expression was investigated using the method of immunohistochemistry (IHC) in a tissue microarray (TMA) incorporating 50 pairs of colon cancer specimens and adjacent normal tissue. In addition, the correlation of FOXJ1 expression with clinicopathological characteristics was evaluated in the other TMA containing 208 cases of colon cancer. Moreover, the influence of regulating FOXJ1 level on the proliferation, migration, and invasion ability of colorectal cancer (CRC) cells was evaluated. RESULTS Increased expression of FOXJ1was significantly associated with clinical stage (p<0.05), metastasis of lymph node (p<0.05), and invasion depth (p<0.001) in colon cancer, suggesting FOXJ1 is a tumor promoter in CRC. Consistently, FOXJ1 overexpression significantly enhanced the proliferation, migration, and invasion of CRC cells, while silencing of FOXJ1 induced the opposite effect. Furthermore, up-regulation of FOXJ1 in SW620 cells markedly inhibited the level of truncated APC and the phosphorylation of β-catenin, while the level of cyclinD1 was decreased. In addition, overexpression of FOXJ1 significantly promoted nuclear translocation of b-catenin in SW620 cells. CONCLUSIONS These findings demonstrate that increased FOXJ1 contributes to the progression of CRC, which might be associated with the promotion effect of b-catenin nuclear translocation. FOXJ1 may be a novel therapeutic target in CRC.

Indexed as

Active Transport, Cell Nucleusbeta CateninCell Line, TumorCell MovementCell ProliferationColorectal NeoplasmsDisease ProgressionForkhead Transcription FactorsGene ExpressionHCT116 CellsHumansImmunohistochemistryTissue Array AnalysisUp-Regulationbeta CateninCTNNB1 protein, humanForkhead Transcription FactorsFOXJ1 protein, human

Identifiers

PMID28209947
PMCPMC5328203
OpenAlexW2588765617

What OpenQuestion holds

Textmetadata
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.