Evidence map›Paper›PMID 18291362›Full record

ArticleEuropean journal of pharmacology2008

Sulindac suppresses beta-catenin expression in human cancer cells.

Anjia Han, Zibo Song, Chang Tong, Dong Hu, Xiuli Bi, Leonard H Augenlicht, Wancai Yang

Abstract read
In one paragraph

Article in European journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. CTNNB1 in neurodevelopmental disorders.Frontiers in psychiatry · 2023
    Review
  7. NSAIDs and Cancer Resolution: New Paradigms beyond Cyclooxygenase.International journal of molecular sciences · 2022
    Review
  8. Wnt/β-catenin signaling in cancers and targeted therapies.Signal transduction and targeted therapy · 2021
    Review
  9. Cellular Plasticity in Breast Cancer Progression and Therapy.Frontiers in molecular biosciences · 2020
    Review
  10. Article
  11. Review
  12. COX-2 inhibitors in NSCLC: never-ending story or misplaced?Translational lung cancer research · 2018
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  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

7 authors at 3 institutions in 1 country.

Anjia HanDepartment of Pathology, University of Illinois at Chicago, Chicago, IL 60612, USA.
Zibo Song
Chang Tong
Dong Hu
Xiuli Bi
Leonard H Augenlicht
Wancai Yang
University of Illinois Chicago · USAlbert Einstein College of Medicine · USCornell University · US

Funding

Intestinal Cancer Chemoprevention: Molecular MechanismsR01CA112081 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI YANG, WANCAI · 2005 to 2009
$1.1M
NCI NIH HHS R01 CA112081NCI NIH HHS R01CA112081
6 · The paper itself

Abstract

Sulindac has been reported to be effective in suppressing tumor growth through the induction of p21WAF1/cip1 in human, animal models of colon cancer and colon cancer cells. In this study, we treated human breast cancer cell line MCF-7 and lung cancer cell line A549 as well as colon cancer cell line SW620 with sulindac to observe the effects of sulindac in other tissue sites. In all cell lines, proliferation was significantly inhibited by sulindac after 24 and 72 h of treatment. Apoptosis was induced by sulindac in both lung cancer cells and colon cancer cells but was not induced in breast cancer cells. Western blots showed that p21 protein level were induced by sulindac in lung cancer cells and colon cancer cells, but not in breast cancer cells. However, the suppression of beta-catenin, a key mediator of Wnt signaling pathway, was seen in all three cell lines with sulindac administration. Further studies revealed that transcriptional activities of beta-catenin were significantly inhibited by sulindac and that the inhibition was sulindac dosage-dependent. The transcriptional targets of beta-catenin, c-myc, cyclin D1 and cdk 4 were also dramatically downregulated. In conclusion, our data demonstrated that the efficacy of sulindac in the inhibition of cell proliferation (rather than the induction of apoptosis) might be through the suppression of beta-catenin pathway in human cancer cells.

Indexed as

Anti-Inflammatory Agents, Non-SteroidalApoptosisbeta CateninBlotting, WesternBreast NeoplasmsCell Line, TumorCell ProliferationColorectal NeoplasmsCyclin D1Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p21Gene Expression Regulation, NeoplasticGenes, ReporterHumansLuciferasesLung NeoplasmsAnti-Inflammatory Agents, Non-Steroidalbeta CateninCDKN1A protein, humanCyclin D1Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p21LuciferasesProto-Oncogene Proteins c-mycSulindac

Identifiers

PMID18291362
PMCPMC2350231
OpenAlexW1975665042

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.