Evidence map›Paper›PMID 27474149›Full record

ArticleMolecular cancer therapeutics2016

Wedelolactone, an Anti-inflammatory Botanical, Interrupts c-Myc Oncogenic Signaling and Synergizes with Enzalutamide to Induce Apoptosis in Prostate Cancer Cells.

Sivalokanathan Sarveswaran, Ritisha Ghosh, Rujul Parikh, Jagadananda Ghosh

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.1field-weighted citation impact, top 10% 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

17 citing papers in PubMed, 41 citations in OpenAlex.

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  13. Prostate cancer: Therapeutic prospect with herbal medicine.Current research in pharmacology and drug discovery · 2021
    Review
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  17. Wedelolactone Acts as Proteasome Inhibitor in Breast Cancer Cells.International journal of molecular sciences · 2017
    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

4 authors at 1 institution in 1 country.

Sivalokanathan SarveswaranVattikuti Urology Institute, Henry Ford Health System, Detroit, Michigan.
Ritisha GhoshVattikuti Urology Institute, Henry Ford Health System, Detroit, Michigan.
Rujul ParikhVattikuti Urology Institute, Henry Ford Health System, Detroit, Michigan.
Jagadananda GhoshVattikuti Urology Institute, Henry Ford Health System, Detroit, Michigan. jghosh1@hfhs.org.
Henry Ford Health System · US

Funding

Regulation of prostate cancer cell survival by 5-lipoxygenase:Role of PKC-epsilonR01CA152334 · NCI · HENRY FORD HEALTH SYSTEM · PI GHOSH, JAGADANANDA · 2011 to 2014
$951k
NCI NIH HHS R01 CA152334
6 · The paper itself

Abstract

The c-Myc gene encodes an oncoprotein transcription factor that is frequently upregulated in almost all cancer types and is the subject of intense investigation for management of cancer because of its pleiotropic effects controlling a spectrum of cellular functions. However, due of its nonenzymatic nature, development of suitable strategies to block its protein-protein or protein-DNA interaction is challenging. Thus, c-Myc has been recognized as an elusive molecular target for cancer control, and various approaches are in development to inhibit c-Myc transcriptional activity. We observed that wedelolactone (WDL), an anti-inflammatory botanical compound, severely downregulates the expression of c-Myc mRNA in prostate cancer cells. Moreover, WDL dramatically decreases the protein level, nuclear accumulation, DNA-binding, and transcriptional activities of c-Myc. c-Myc is a transforming oncogene widely expressed in prostate cancer cells and is critical for maintaining their transformed phenotype. Interestingly, WDL was found to strongly affect the viability of Myc-activated prostate cancer cells and completely block their invasion as well as soft agar colony formation in vitro WDL was also found to downregulate c-Myc in vivo in nude mice xenografts. Moreover, WDL synergizes with enzalutamide to decrease the viability of androgen-sensitive prostate cancer cells via induction of apoptosis. These findings reveal a novel anticancer mechanism of the natural compound WDL, and suggest that the oncogenic function of c-Myc in prostate cancer cells can be effectively downregulated by WDL for the development of a new therapeutic strategy against Myc-driven prostate cancer. Mol Cancer Ther; 15(11); 2791-801. ©2016 AACR.

Indexed as

AnimalsApoptosisBenzamidesCell Line, TumorCell SurvivalCoumarinsDisease Models, AnimalDrug SynergismGene Expression Regulation, NeoplasticHumansMaleMiceNeoplastic Stem CellsNitrilesPhenylthiohydantoinProstatic NeoplasmsBenzamidesCoumarinsenzalutamideNitrilesPhenylthiohydantoinProto-Oncogene Proteins c-mycwedelolactone

Identifiers

PMID27474149
PMCPMC5096967
OpenAlexW2498011087

What OpenQuestion holds

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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.