Evidence map›Paper›PMID 24912879›Full record

ArticleJournal of cellular and molecular medicine2014

Epigenetic silencing of DACH1 induces the invasion and metastasis of gastric cancer by activating TGF-β signalling.

Wenji Yan, Kongming Wu, James G Herman, Malcolm V Brock, Yusen Zhou, Youyong Lu, Zhiqian Zhang, Yunsheng Yang, Mingzhou Guo

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Epigenetic heterogeneity in cancer.Biomarker research · 2019
    Review
  10. World journal of gastroenterology · 2018
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Estrogen receptor β, a regulator of androgen receptor signaling in the mouse ventral prostate.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  17. Article
  18. Article
  19. Article
  20. 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 7 institutions in 2 countries.

Wenji YanInstitute of Digestive Diseases, Chinese PLA General Hospital, Beijing, China.
Kongming Wu
James G Herman
Malcolm V Brock
Yusen Zhou
Youyong Lu
Zhiqian Zhang
Yunsheng Yang
Mingzhou Guo
Chinese PLA General Hospital · CNInstitute of Microbiology · CNJohns Hopkins Medicine · USJohns Hopkins University · USPeking University · CNPeking University Cancer Hospital · CNTongji Hospital · CN

Funding

MIF in progression and treatment of ALDU01AA020821 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI NAGY, LAURA E. · 2012 to 2016
$2.1M
Corticostriatal networks and NMDAR mediation of habitual and flexible actionK22AA020303 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI BRIGMAN, JONATHAN L · 2011 to 2013
$486k
NIAAA NIH HHS K22 AA020303NIAAA NIH HHS U01 AA020821
6 · The paper itself

Abstract

Gastric cancer (GC) is the fourth most common malignancy in males and the fifth most common malignancy in females worldwide. DACH1 is frequently methylated in hepatic and colorectal cancer. To further understand the regulation and mechanism of DACH1 in GC, eight GC cell lines, eight cases of normal gastric mucosa, 98 cases of primary GC and 50 cases of adjacent non-tumour tissues were examined. Methylation-specific PCR, western blot, transwell assay and xenograft mice were used in this study. Loss of DACH1 expression correlated with promoter region methylation in GC cells, and re-expression was induced by 5-Aza-2'-deoxyazacytidine. DACH1 is methylated in 63.3% (62/98) of primary GC and 38% (19/50) of adjacent non-tumour tissues, while no methylation was found in normal gastric mucosa. Methylation of DACH1 correlated with reduced expression of DACH1 (P < 0.01), late tumour stage (stage III/IV) (P < 0.01) and lymph node metastasis (P < 0.05). DACH1 expression inhibited epithelial-mesenchymal transition and metastasis by inhibiting transforming growth factor (TGF)-β signalling and suppressed GC cell proliferation through inducing G2/M phase arrest. The tumour size is smaller in DACH1-expressed BGC823 cell xenograft mice than in unexpressed group (P < 0.01). Restoration of DACH1 expression also sensitized GC cells to docetaxel. These studies suggest that DACH1 is frequently methylated in human GC and expression of DACH1 was controlled by promoter region methylation. DACH1 suppresses GC proliferation, invasion and metastasis by inhibiting TGF-β signalling pathways both in vitro and in vivo. Epigenetic silencing DACH1 may induce GC cells' resistance to docetaxel.

Indexed as

Epigenesis, GeneticAnimalsBlotting, WesternCell LineCell Line, TumorCell MovementCell SurvivalDNA MethylationDocetaxelDose-Response Relationship, DrugEye ProteinsFemaleHumansMaleMice, Inbred BALB CMice, NudeDACH1 protein, humanDocetaxelEye ProteinsTaxoidsTranscription FactorsTransforming Growth Factor betachemosensitive markerDACH1DNA methylationdocetaxelgastric cancerinvasionmetastasis

Identifiers

PMID24912879
PMCPMC4302654
OpenAlexW2093947772

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.