Evidence map›Paper›PMID 28521288›Full record

ArticleOncotarget2017

Hypermethylation of NDN promotes cell proliferation by activating the Wnt signaling pathway in colorectal cancer.

Yu-Han Hu, Qing Chen, Yan-Xia Lu, Jian-Ming Zhang, Chun Lin, Fan Zhang, Wen-Juan Zhang, Xiao-Min Li, Wei Zhang, Xue-Nong Li

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 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
1.1field-weighted citation impact, top 23% 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, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  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

10 authors at 2 institutions in 1 country.

Yu-Han HuDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Qing ChenDepartment of Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yan-Xia LuDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Jian-Ming ZhangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Chun LinDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Fan ZhangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Wen-Juan ZhangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Xiao-Min LiDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Wei ZhangDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Xue-Nong LiDepartment of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Southern Medical University · CNNanfang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The progression of CRC is a multistep process involving several genetic changes or epigenetic modifications. NDN is a member of the MAGE family, encoding a protein that generally suppresses cell proliferation and acting as a transcriptional repressor. Immunohistochemical staining revealed that the expression of NDN was significantly down-regulated in CRC tissues compared with normal tissues and the down-regulation of NDN in CRC could reflect the hypermethylation of the NDN promoter. Treatment of the CRC cell line SW480 with the demethylating agent 5-Aza-CdR restored the NDN expression level. The down-regulation of NDN was closely related to poor differentiation, advanced TNM stage and poor prognosis of CRC. The inhibition of NDN promoted CRC cell proliferation by enriching cells in the S phase. Furthermore, we observed that NDN binds to the GN box in the promoter of LRP6 to attenuate LRP6 transcription and inhibit the Wnt signaling pathway in CRC. In conclusion, our study revealed that the hypermethylation of NDN promotes cell proliferation by activating the Wnt signaling pathway through directly increasing the transcription of LRP6 in CRC. These findings might provide a new theoretical basis for the pathogenesis of CRC and facilitate the development of new therapeutic strategies against CRC.

Indexed as

AnimalsAzacitidineCarcinogenesisCell MovementCell ProliferationColonic NeoplasmsColorectal NeoplasmsDNA MethylationEpigenesis, GeneticFemaleGene Expression Regulation, NeoplasticHCT116 CellsHT29 CellsHumansLow Density Lipoprotein Receptor-Related Protein-6MaleAzacitidineLow Density Lipoprotein Receptor-Related Protein-6LRP6 protein, humanNDN protein, humanRNA, Small InterferingTumor Suppressor Proteinscolorectal cancerLRP6NDNproliferationWnt signaling pathway

Identifiers

PMID28521288
PMCPMC5542259
OpenAlexW2611167721

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.