Evidence map›Paper›PMID 22904674›Full record

ArticleNeoplasia (New York, N.Y.)2012

Epigenetic silencing of HOPX promotes cancer progression in colorectal cancer.

Hiroshi Katoh, Keishi Yamashita, Mina Waraya, Ofer Margalit, Akira Ooki, Hideaki Tamaki, Hiroyuki Sakagami, Kenichi Kokubo, David Sidransky, Masahiko Watanabe

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. The Ketogenic Diet in Colorectal Cancer: A Means to an End.International journal of molecular sciences · 2023
    Review
  11. Review
  12. Review
  13. Article
  14. HOPXAmerican journal of physiology. Gastrointestinal and liver physiology · 2021
    Article
  15. Article
  16. Article
  17. Review
  18. Diagnostic and prognostic values of forkhead box D4 gene in colonic adenocarcinoma.International journal of clinical and experimental pathology · 2020
    Article
  19. Article
  20. Preservation of reserve intestinal epithelial stem cells following severe ischemic injury.American journal of physiology. Gastrointestinal and liver physiology · 2019
    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

10 authors at 4 institutions in 3 countries.

Hiroshi KatohDepartment of Surgery, Kitasato University School of Medicine, Sagamihara, Japan.
Keishi Yamashita
Mina Waraya
Ofer Margalit
Akira Ooki
Hideaki Tamaki
Hiroyuki Sakagami
Kenichi Kokubo
David Sidransky
Masahiko Watanabe
Kitasato University · JPJohns Hopkins Medicine · USSheba Medical Center · ILThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Homeodomain-only protein X (HOPX)-β promoter methylation was recently shown to be frequent in human cancers and was suggested as tumor suppressor gene in esophageal and gastric cancer. The aim of this study was to investigate the mechanistic roles of HOPX-β promoter methylation and its clinical relevance in colorectal cancer (CRC). HOPX-β promoter methylation was assessed in human CRC cell lines and 294 CRC tissues. HOPX mRNA and protein levels were measured in relation to HOPX-β promoter methylation. The effects of forced HOPX expression on tumorigenesis were studied using in vitro and in vivo assays. The association between HOPX-β promoter methylation and clinical relevance of CRC patients was determined. HOPX-β promoter methylation is cancer-specific and frequently found in CRC cell lines and tissues, resulting in the down-regulation of HOPX mRNA and protein levels. In CRC cell lines, forced expression of HOPX suppressed proliferation, invasion, and anchorage-independent growth. DNA microarray analyses suggested critical downstream genes that are associated with cancer cell proliferation, invasion or angiogenesis. In a mouse xenograft model, HOPX inhibited tumorigenesis and angiogenesis. Finally, HOPX-β promoter methylation was associated with worse prognosis of stage III CRC patients (hazard ratio= 1.40, P = .035) and also with poor differentiation (P = .014). In conclusion, HOPX-β promoter methylation is a frequent and cancer-specific event in CRC progression. This epigenetic alteration may have clinical ramifications in the diagnosis and treatment of CRC patients.

Indexed as

Gene SilencingAnimalsCell Line, TumorCell Transformation, NeoplasticColorectal NeoplasmsCpG IslandsDisease ProgressionDNA MethylationGene Expression ProfilingGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHomeodomain ProteinsHumansMaleMiceMice, Inbred BALB CHomeodomain ProteinsHOPX protein, humanTumor Suppressor Proteins

Identifiers

PMID22904674
PMCPMC3421953
OpenAlexW1955847844

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.