Evidence map›Paper›PMID 26673922›Full record

ArticleBMC cancer2015

Sulindac sulfide inhibits colon cancer cell growth and downregulates specificity protein transcription factors.

Xi Li, Satya S Pathi, Stephen Safe

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Unboxing the molecular modalities of mutagens in cancer.Environmental science and pollution research international · 2022
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

3 authors at 2 institutions in 1 country.

Xi LiDepartment of Veterinary Physiology & Pharmacology, Texas A&M University, College Station, TX, 77843-4466, USA.
Satya S PathiOklahoma Medical Research Foundation, 825 NE 13th St., Oklahoma City, OK, 73104, USA.
Stephen SafeDepartment of Veterinary Physiology & Pharmacology, Texas A&M University, College Station, TX, 77843-4466, USA. ssafe@cvm.tamu.edu.
Texas A&M University · USOklahoma Medical Research Foundation · US

Funding

TARGETED GENOMICS FACILITY COREP30ES023512 · NIEHS · TEXAS A&M AGRILIFE RESEARCH · PI DEUTZ, NICOLAAS E · 2014 to 2017
$3.3M
NIEHS NIH HHS P30 ES023512NIEHS NIH HHS P30-ES023512
6 · The paper itself

Abstract

backgroundSpecificity protein (Sp) transcription factors play pivotal roles in maintaining the phenotypes of many cancers. We hypothesized that the antineoplastic effects of sulindac and its metabolites were due, in part, to targeting downregulation of Sp transcription factors.

methodsThe functional effects of sulindac, sulindac sulfone and sulindac sulfide on colon cancer cell proliferation were determined by cell counting. Effects of these compounds on expression of Sp1, Sp3, Sp4 and pro-oncogenic Sp-regulated genes were determined by western blot analysis of whole cell lysates and in transient transfection assays using GC-rich constructs.

resultsSulindac and its metabolites inhibited RKO and SW480 colon cancer cell growth and the order of growth inhibitory potency was sulindac sulfide>>sulindac sulfone>sulindac. Treatment of SW480 and RKO cells with sulindac sulfide downregulated expression of Sp1, Sp3 and Sp4 proteins. Sulindac sulfide also decreased expression of several Sp-regulated genes that are critical for cancer cell survival, proliferation and angiogenesis and these include survivin, bcl-2, epidermal growth factor receptor (EGFR), cyclin D1, p65 subunit of NFκB and vascular endothelial growth factor (VEGF). Sulindac sulfide also induced reactive oxygen species (ROS) and decreased the level of microRNA-27a in colon cancer cells, which resulted in the upregulation of the Sp-repressor ZBTB10 and this resulted in downregulation of Sp proteins.

conclusionsThe results suggest that the cancer chemotherapeutic effects of sulindac in colon cancer cells are due, in part, to its metabolite sulindac sulfide which downregulates Sp transcription factors and Sp-regulated pro-oncogenic gene products.

Indexed as

Antineoplastic AgentsBlotting, WesternCell Line, TumorCell ProliferationColonic NeoplasmsDown-RegulationFlow CytometryGene Expression Regulation, NeoplasticHumansReal-Time Polymerase Chain ReactionSp Transcription FactorsSulindacAntineoplastic AgentsSp Transcription FactorsSulindacsulindac sulfide

Identifiers

PMID26673922
PMCPMC4682223
OpenAlexW2202626070

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.