Evidence map›Paper›PMID 19204913›Full record

ArticleThe Prostate2009

Effects of the sesquiterpene lactone parthenolide on prostate tumor-initiating cells: An integrated molecular profiling approach.

Brian T Kawasaki, Elaine M Hurt, Madhuri Kalathur, Maria Ana Duhagon, John A Milner, Young S Kim, William L Farrar

Open access · greenAbstract read
In one paragraph

Article in The Prostate, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

53 citing papers in PubMed, 100 citations in OpenAlex.

  1. Serum Metabolomic Response to Low- and High-Dose Vitamin E Supplementation in Two Randomized Controlled Trials.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2020
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  16. Sesquiterpene lactones from shoot culture ofResearch in pharmaceutical sciences · 2019
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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

7 authors at 3 institutions in 2 countries.

Brian T KawasakiCancer Stem Cell Section, Laboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute at Frederick (NCI-Frederick), National Institutes of Health,1050Boyles Street, Frederick, MD 21702, USA.
Elaine M Hurt
Madhuri Kalathur
Maria Ana Duhagon
John A Milner
Young S Kim
William L Farrar
National Institutes of Health · USCenter for Cancer Research · USFrederick National Laboratory for Cancer Research · US

Funding

Characterization of Cancer Stem CellsZIABC010794 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI FARRAR, WILLIAM · 2009 to 2012
$3.2M
Characterization of Cancer Stem CellsZ01BC010794 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI FARRAR, WILLIAM · 2007 to 2008
$1.3M
Molecular Mechanisms of Growth Factor Modulated ProliferationZIABC010253 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI FARRAR, WILLIAM · 2009 to 2012
$795k
Intramural NIH HHS Z01 BC010794NCI NIH HHS N01 CO012400NCI NIH HHS N01 CO-12400
6 · The paper itself

Abstract

Recent evidence suggests tumor-initating cells (TICs), also called cancer stem cells, are responsible for tumor initiation and progression; therefore, they represent an important cell population for development of future anti-cancer therapies. In this study, we show that the sesquiterpene lactone parthenolide (PTL) is cytotoxic to prostate TICs isolated from prostate cancer cell lines: DU145, PC3, VCAP, and LAPC4, as well as primary prostate TICs. Furthermore, PTL inhibited TIC-driven tumor formation in mouse xenografts. Using an integrated molecular profiling approach encompassing proteomics, profiles of activated transcription factors and genomics we ascertained the effects of PTL on prostate cancer cells. In addition to the previously described effects of PTL, we determined that the non-receptor tyrosine kinase src, and many src signaling components, including: Csk, FAK, beta1-arrestin, FGFR2, PKC, MEK/MAPK, CaMK, ELK-1, and ELK-1-dependent genes are novel targets of PTL action. Furthermore, PTL altered the binding of transcription factors important in prostate cancer including: C/EBP-alpha, fos related antigen-1 (FRA-1), HOXA-4, c-MYB, SNAIL, SP1, serum response factor (SRF), STAT3, X-box binding protein-1 (XBP1), and p53. In summary, we show PTL is cytotoxic to prostate TICs and describe the molecular events of PTL-mediated cytotoxicity. Therefore, PTL represents a promising therapeutic for prostate cancer treatment.

Indexed as

AnimalsAntigens, CDCell Line, TumorFlow CytometryGene Expression ProfilingHumansHyaluronan ReceptorsMaleMiceNeoplasm ProteinsOligonucleotide Array Sequence AnalysisProstateProstatic NeoplasmsRNA, NeoplasmSesquiterpenesTranscription, GeneticAntigens, CDHyaluronan ReceptorsNeoplasm ProteinsparthenolideRNA, NeoplasmSesquiterpenes

Identifiers

PMID19204913
PMCPMC2700306
OpenAlexW2115214814

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.