Evidence map›Paper›PMID 22159228›Full record

ArticleCarcinogenesis2012

Effects of S-adenosylmethionine and methylthioadenosine on inflammation-induced colon cancer in mice.

Tony W H Li, Heping Yang, Hui Peng, Meng Xia, José M Mato, Shelly C Lu

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 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
1.5field-weighted citation impact, top 18% 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, 70 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Review
  7. Article
  8. Article
  9. The Crucial Roles of Intermediate Metabolites in Cancer.Cancer management and research · 2021
    Review
  10. DNA Methylation Patterns inEnvironmental health perspectives · 2021
    Article
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  12. Review
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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

6 authors at 4 institutions in 2 countries.

Tony W H LiDivision of Gastroenterology and Liver Diseases, University of Southern California Research Center for Liver Diseases, University of Southern California-University of California, Los Angeles, CA 90033, USA.
Heping Yang
Hui Peng
Meng Xia
José M Mato
Shelly C Lu
University of California, Los Angeles · USCIC bioGUNE · ESSouthern California University for Professional Studies · USUniversity of Southern California · US

Funding

USC RESEARCH CENTER FOR LIVER DISEASES: PILOT PROGRAMSP30DK048522 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KAPLOWITZ, NEIL · 1995 to 2020
$21.8M
Role of MAT and SAMe in Colon Cancer Pathogenesis and TreatmentR01AT004896 · NCCIH · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LU, SHELLY CHI-LOO · 2008 to 2012
$2.0M
NCCIH NIH HHS AT004896NCCIH NIH HHS R01 AT004896NIDDK NIH HHS P30 DK048522NIDDK NIH HHS P30DK48522
6 · The paper itself

Abstract

Chronic inflammation is an underlying risk factor for colon cancer. Tumor necrosis factor alpha (TNF-α) plays a critical role in the development of inflammation-induced colon cancer in a mouse model. S-adenosylmethionine (SAMe) and its metabolite methylthioadenosine (MTA) can inhibit lipopolysaccharide-induced TNF-α expression in macrophages. The aim of this work was to examine whether SAMe and MTA are effective in preventing inflammation-induced colon cancer and if so identify signaling pathways affected. Balb/c mice were treated with azoxymethane (AOM) and dextran sulfate sodium to induce colon cancer. Two days after AOM treatment, mice were divided into three groups: vehicle control, SAMe or MTA. Tumor load, histology, immunohistochemistry, gene and protein expression were determined. SAMe and MTA treatment reduced tumor load by ∼40%. Both treatments raised SAMe and MTA levels but MTA also raised S-adenosylhomocysteine levels. MTA treatment prevented the induction of many genes known to play pathogenetic roles in this model except for TNF-α and inducible nitric oxide synthase (iNOS). SAMe also had no effect on TNF-α or iNOS and was less inhibitory than MTA on the other genes. In vivo, both treatments induced apoptosis but inhibited proliferation, β-catenin, nuclear factor kappa B activation and interleukin (IL) 6 signaling. Effect of SAMe and MTA on IL-6 signaling was examined using Colo 205 colon cancer cells. In these cells, SAMe and MTA inhibited IL-6-induced IL-10 expression. MTA also inhibited IL-10 transcription and signal transducer and activator of transcription 3 activation. In conclusion, SAMe and MTA reduced inflammation-induced colon cancer and inhibited several pathways important in colon carcinogenesis.

Indexed as

AnimalsApoptosisAzoxymethanebeta CateninCell ProliferationCell Transformation, NeoplasticChemopreventionColonic NeoplasmsDextran SulfateInflammationInterleukin-10Interleukin-6MaleMiceMice, Inbred BALB CNF-kappa B5'-methylthioadenosine phosphorylaseAzoxymethanebeta CateninDextran SulfateInterleukin-10Interleukin-6NF-kappa BNitric Oxide Synthase Type IINos2 protein, mouseProto-Oncogene Proteins c-aktPurine-Nucleoside PhosphorylaseS-AdenosylhomocysteineS-AdenosylmethionineStat3 protein, mouseSTAT3 Transcription FactorTumor Necrosis Factor-alpha

Identifiers

PMID22159228
PMCPMC3279046
OpenAlexW2146881937

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.