Evidence map›Paper›PMID 21152119›Full record

ArticleInternational journal of biological sciences2010

S-adenosylmethionine inhibits the growth of cancer cells by reversing the hypomethylation status of c-myc and H-ras in human gastric cancer and colon cancer.

Jin Luo, Yan-Ni Li, Fei Wang, Wei-Ming Zhang, Xin Geng

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

70 citing papers in PubMed, 117 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Silencing of MAT2A inhibits gastric cancer cell proliferation, migration, and invasion through activation of the p53 pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Omics-based molecular classifications empowering in precision oncology.Cellular oncology (Dordrecht, Netherlands) · 2024
    Review
  13. Antitumoral Activity of the Universal Methyl DonorMolecules (Basel, Switzerland) · 2024
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

10 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Jin LuoDepartment of biochemistry, Tianjin Medical University, Tianjin, 300070 China.
Yan-Ni Li
Fei Wang
Wei-Ming Zhang
Xin Geng
Tianjin Medical University · CNTianjin Stomatological Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A global DNA hypomethylation might activate oncogene transcription, thus promoting carcinogenesis and tumor development. S-Adenosylmethionine (SAM) serves as a major methyl donor in biological transmethylation events. The object of this study is to explore the influence of SAM on the status of methylation at the promoter of the oncogenes c-myc, H-ras and tumor-suppressor gene p16 (INK4a), as well as its inhibitory effect on cancer cells. The results indicated that SAM treatment inhibited cell growth in gastric cancer cells and colon cancer cells, and the inhibition efficiency was significantly higher than that in the normal cells. Under standard growth conditions, C-myc and H-ras promoters were hypomethylated in gastric cancer cells and colon cancer cells. SAM treatment resulted in a heavy methylation of these promoters, which consequently downregulated mRNA and protein levels. In contrast, there was no significant difference in mRNA and protein levels of p16 (INK4a) with and without SAM treatment. SAM can effectively inhibit the tumor cells growth by reversing the DNA hypomethylation on promoters of oncogenes, thus down-regulating their expression. With no influence on the expression of the tumor suppressor genes, such as P16, SAM could be used as a potential drug for cancer therapy.

Indexed as

Blotting, WesternCell Line, TumorCell ProliferationCyclin-Dependent Kinase Inhibitor p16DNA MethylationFluorescent Antibody TechniqueGenes, rasHT29 CellsHumansPolymerase Chain ReactionPromoter Regions, GeneticProto-Oncogene Proteins c-mycReverse Transcriptase Polymerase Chain ReactionS-AdenosylmethionineStomach NeoplasmsCyclin-Dependent Kinase Inhibitor p16MYC protein, humanProto-Oncogene Proteins c-mycS-Adenosylmethioninecancer therapyepigeneticsgastric cancerhypomethylationS-Adenosylmethionine

Identifiers

PMID21152119
PMCPMC2999854
OpenAlexW2093930180

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.