Evidence map›Paper›PMID 20978115›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2010

Thiocolchicoside exhibits anticancer effects through downregulation of NF-κB pathway and its regulated gene products linked to inflammation and cancer.

Simone Reuter, Sahdeo Prasad, Kanokkarn Phromnoi, Jayaraj Ravindran, Bokyung Sung, Vivek R Yadav, Ramaswamy Kannappan, Madan M Chaturvedi, Bharat B Aggarwal

Open access · bronzeAbstract read
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.2field-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

25 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
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  9. Review
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  12. Benzodiazepine partially reverses tonic-clonic seizures induced by thiocolchicoside.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2022
    Article
  13. Article
  14. Overcoming cancer therapeutic bottleneck by drug repurposing.Signal transduction and targeted therapy · 2020
    Review
  15. Article
  16. Article
  17. Protective Role of Dietary Berries in Cancer.Antioxidants (Basel, Switzerland) · 2016
    Review
  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

9 authors at 2 institutions in 2 countries.

Simone ReuterCytokine Research Laboratory, Department of Experimental Therapeutics, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Sahdeo Prasad
Kanokkarn Phromnoi
Jayaraj Ravindran
Bokyung Sung
Vivek R Yadav
Ramaswamy Kannappan
Madan M Chaturvedi
Bharat B Aggarwal
The University of Texas MD Anderson Cancer Center · USUniversity of Delhi · IN

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
TARGETING NF-KB ACTIVATION IN REGULATION OF SYMPTOMS IN PATIENTS WITH MULTIPLEP01CA124787 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI REUBEN, JAMES MARTIN · 2008 to 2012
$10.6M
NCI NIH HHS CA-124787-01A2NCI NIH HHS CA-16 672NCI NIH HHS P01 CA124787
6 · The paper itself

Abstract

The discovery of new uses for older, clinically approved drugs is one way to expedite drug development for cancer. Thiocolchicoside, a semisynthetic colchicoside from the plant Gloriosa superba, is a muscle relaxant and used to treat rheumatologic and orthopedic disorders because of its analgesic and anti-inflammatory mechanisms. Given that activation of the transcription factor NF-κB plays a major role in inflammation and tumorigenesis, we postulated that thiocolchicoside would inhibit NF-κB and exhibit anticancer effects through the modulation of NF-κB-regulated proteins. We show that thiocolchicoside inhibited proliferation of leukemia, myeloma, squamous cell carcinoma, breast, colon, and kidney cancer cells. Formation of tumor colonies was also suppressed by thiocolchicoside. The colchicoside induced apoptosis, as indicated by caspase-3 and poly(ADP-ribose) polymerase cleavage, and suppressed the expression of cell survival [e.g., Bcl-2, X-linked inhibitor of apoptosis (XIAP), MCL-1, bcl-xL, cIAP-1, cIAP-2, and cFLIP] proteins. Cell proliferation biomarkers such as c-MYC and phosphorylation of phosphoinositide 3-kinase and glycogen synthase kinase 3β were also blocked by thiocolchicoside. Because most cell survival and proliferation gene products are regulated by NF-κB, we studied the effect of thiocolchicoside on this transcription factor and found that thiocolchicoside inhibited NF-κB activation, degradation of inhibitory κBα (IκBα), IκBα ubiquitination, and phosphorylation, abolished the activation of IκBα kinase, and suppressed p65 nuclear translocation. This effect of thiocolchicoside on the NF-κB pathway led to inhibition of NF-κB reporter activity and cyclooxygenase-2 promoter activity. Our results indicate that thiocolchicoside exhibits anticancer activity through inhibition of NF-κB and NF-κB-regulated gene products, which provides novel insight into a half-century old drug.

Indexed as

Antineoplastic AgentsBlotting, WesternCell Line, TumorColchicineDown-RegulationElectrophoretic Mobility Shift AssayHumansInflammationNeoplasmsNF-kappa BSignal TransductionAntineoplastic AgentsColchicineNF-kappa Bthiocolchicoside

Identifiers

PMID20978115
PMCPMC3142676
OpenAlexW2112323960

What OpenQuestion holds

Textmetadata
LicenceTDM
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.