Evidence map›Paper›PMID 18403754›Full record

ArticleStem cells (Dayton, Ohio)2008

Platelet-derived growth factor-D overexpression contributes to epithelial-mesenchymal transition of PC3 prostate cancer cells.

Dejuan Kong, Zhiwei Wang, Sarah H Sarkar, Yiwei Li, Sanjeev Banerjee, Allen Saliganan, Hyeong-Reh Choi Kim, Michael L Cher, Fazlul H Sarkar

Abstract read
In one paragraph

Article in Stem cells (Dayton, Ohio), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
–field-weighted citation impact
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

84 citing papers in PubMed.

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24 more citing papers are in PubMed but not listed here.

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.

Dejuan KongDepartment of Pathology, Karmanos Cancer Institute, Wayne State University School of Medicine, Detroit, Michigan 48201, USA.
Zhiwei Wang
Sarah H Sarkar
Yiwei Li
Sanjeev Banerjee
Allen Saliganan
Hyeong-Reh Choi Kim
Michael L Cher
Fazlul H Sarkar

Funding

Novel Targets of Indoles in Prostate CancerR01CA108535 · NCI · WAYNE STATE UNIVERSITY · PI SARKAR, FAZLUL H. · 2004 to 2014
$2.7M
FoxM1: A molecular target in pancreatic cancerR01CA132794 · NCI · WAYNE STATE UNIVERSITY · PI SARKAR, FAZLUL H. · 2009 to 2013
$1.5M
Mechanistic Role of miRNAs and Their Targets in Prostate Cancer AggressivenessR01CA164318 · NCI · WAYNE STATE UNIVERSITY · PI SARKAR, FAZLUL H. · 2012 to 2015
$1.3M
NCI NIH HHS 5R01-CA108535-04NCI NIH HHS R01 CA108535NCI NIH HHS R01 CA132794NCI NIH HHS R01 CA164318
6 · The paper itself

Abstract

The majority of human malignancies are believed to have epithelial origin, and the progression of cancer is often associated with a transient process named epithelial-mesenchymal transition (EMT). EMT is characterized by the loss of epithelial markers and the gain of mesenchymal markers that are typical of "cancer stem-like cells," which results in increased cell invasion and metastasis in vivo. Therefore, it is important to uncover the mechanistic role of factors that may induce EMT in cancer progression. Studies have shown that platelet-derived growth factor (PDGF) signaling contributes to EMT, and more recently, PDGF-D has been shown to regulate cancer cell invasion and angiogenesis. However, the mechanism by which PDGF-D promotes invasion and metastases and whether it is due to the acquisition of EMT phenotype remain elusive. For this study, we established stably transfected PC3 cells expressing high levels of PDGF-D, which resulted in the significant induction of EMT as shown by changes in cellular morphology concomitant with the loss of E-cadherin and zonula occludens-1 and gain of vimentin. We also found activation of mammalian target of rapamycin and nuclear factor-kappaB, as well as Bcl-2 overexpression, in PDGF-D PC3 cells, which was associated with enhanced adhesive and invasive behaviors. More importantly, PDGF-D-overexpressing PC3 cells showed tumor growth in SCID mice much more rapidly than PC3 cells. These results provided a novel mechanism by which PDGF-D promotes EMT, which in turn increases tumor growth, and these results further suggest that PDGF-D could be a novel therapeutic target for the prevention and/or treatment of prostate cancer. Disclosure of potential conflicts of interest is found at the end of this article.

Indexed as

Epithelial CellsGene Expression Regulation, NeoplasticHumansLymphokinesMaleMesodermNeoplasm InvasivenessPlasmidsPlatelet-Derived Growth FactorPolymerase Chain ReactionProstatic NeoplasmsRNA, NeoplasmRNA, Small InterferingTransfectionLymphokinesPDGFD protein, humanPlatelet-Derived Growth FactorRNA, NeoplasmRNA, Small Interfering

Identifiers

PMID18403754
PMCPMC3766351

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.