Evidence map›Paper›PMID 22522911›Full record

ArticleEpigenetics2012

Silencing of Wnt5a during colon cancer metastasis involves histone modifications.

Qian Li, Hong Chen

Open access · bronzeAbstract read
In one paragraph

Article in Epigenetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 48 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. WNT5B in Physiology and Disease.Frontiers in cell and developmental biology · 2021
    Review
  14. Review
  15. Article
  16. Review
  17. Epigenetic Biomarkers in Colorectal Cancer.Molecular diagnosis & therapy · 2017
    Review
  18. Review
  19. WNT-5A: signaling and functions in health and disease.Cellular and molecular life sciences : CMLS · 2016
    Review
  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

2 authors at 1 institution in 1 country.

Qian LiDepartment of Food Science and Human Nutrition; University of Illinois at Urbana-Champaign, Urbana, IL, USA.
Hong Chen
Urbana University · US

Funding

Pharmacokinetics, Bioavailability, and Metabolism/Daniel R. DoergeP50AT006268 · NCCIH · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI HELFERICH, WILLIAM G · 2010 to 2015
$7.6M
NCCIH NIH HHS P50 AT006268NCCIH NIH HHS P50AT006268
6 · The paper itself

Abstract

Colorectal cancer (CRC) is the third most common cancer in the United States. Approximately 90% of colon cancer deaths arise from the metastasis of primary tumors. Aberrant expression of Wnt5a, one of the WNT signaling factors, has been reported during colon cancer development and progression. We found that both mRNA and protein expression of Wnt5a were decreased in the highly metastatic human colon cancer cell line SW620 compared with the non-metastatic human colon cancer cell SW480. This study tested the hypothesis that the silencing of Wnt5a in metastatic human colon cancer cells is related to altered epigenetic modifications. Wnt5a expression was not responsive to DNA methyltransferase inhibitor 5-aza-cytidine treatment. However, histone deacetylase (HDAC) inhibitors trichostatin A (TSA) and sodium butyrate (NaBt) significantly increased Wnt5a mRNA expression in SW620. Importantly, lower transcription of Wnt5a in SW620 than SW480 corresponded to multiple histone modifications, including lower levels of acetylated histone H3, H4 and H3K4me2 and higher levels of H3K27me3 in the promoter region. The increase of H3Ac, H4Ac and H3K4me2 after NaBt treatment in SW620 confirmed the involvement of histone modifications in the transcriptional regulation of Wnt5a. Additionally, NaBt treatment increased β-catenin signaling and diminished the difference in cell adhesion ability between non-metastatic SW480 and metastatic SW620, suggesting that the HDAC inhibitor plays critical roles in the WNT signaling pathway and cell physiology that relate to metastasis. In conclusion, our study suggests the importance of Wnt5a in colon cancer metastasis and also indicates that Wnt5a silencing in the highly invasive human colon cancer cell line might result from transcriptional regulation of the gene by histone modifications.

Indexed as

Gene SilencingAzacitidineCell Line, TumorColonic NeoplasmsDNA Modification MethylasesGene Expression Regulation, NeoplasticHistone DeacetylasesHistonesHumansHydroxamic AcidsNeoplasm MetastasisProtein Processing, Post-TranslationalProto-Oncogene ProteinsWnt-5a ProteinWnt Proteins5-aza-2'-deoxycytidine-5'-monophosphateAzacitidineDNA Modification MethylasesHistone DeacetylasesHistonesHydroxamic AcidsProto-Oncogene Proteinstrichostatin AWnt-5a ProteinWNT5A protein, humanWnt Proteins

Identifiers

PMID22522911
PMCPMC3398984
OpenAlexW1978372068

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.