Evidence map›Paper›PMID 16302260›Full record

ArticleThe Prostate2006

Antitumor activity and downregulation of pro-angiogenic molecules in human prostate cancer cells by a novel thiazolidione compound.

Fuminori Teraishi, Shuhong Wu, Satoshi Inoue, Lidong Zhang, John J Davis, Wei Guo, Fengqin Dong, Bingliang Fang

Abstract read
In one paragraph

Article in The Prostate, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Fuminori TeraishiDepartment of Thoracic and Cardiovascular Surgery, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA.
Shuhong Wu
Satoshi Inoue
Lidong Zhang
John J Davis
Wei Guo
Fengqin Dong
Bingliang Fang

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI GIBBONS, DON LYNN · 1996 to 2024
$57.4M
Oncolytic adenovector-mediated TRAIL gene therapy for cancersR01CA092487 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI FANG, BINGLIANG · 2002 to 2011
$2.4M
Expression of Proapoptotic Genes for Cancer TherapyR01CA098582 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI FANG, BINGLIANG · 2003 to 2006
$1.3M
Novel CTD inhibitors with synthetic lethality to oncogenic Ras for cancer therapyR01CA124951 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI FANG, BINGLIANG · 2010 to 2013
$1.2M
NCI NIH HHS CA 16672NCI NIH HHS CA 70907NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA070907NCI NIH HHS R01 CA092487NCI NIH HHS R01 CA098582NCI NIH HHS R01 CA124951NIAID NIH HHS R01 CA 092487-01AINIAID NIH HHS R01 CA 098582-01AI
6 · The paper itself

Abstract

backgroundCurrent treatments for prostate cancer are effective in many patients with locally advanced disease, but many of these patients eventually have recurrence. It is therefore important to develop alternative therapeutic agents with improved efficacy and tolerability. We recently identified a synthetic thiazolidin compound, 5-(2,4-dihydroxybenzylidene)-2-(phenylimino)-1,3-thiazolidione (DBPT), that induces apoptosis in human colon cancer cells, independent of p53 and P-glycoprotein status. Here, we investigated the antitumor properties and mechanisms of action of this compound in human prostate cancer cell lines.

methodsThe effect of DBPT on cell-cycle progression and apoptosis in LNCaP and DU145 cells was examined by flow cytometry and Western blotting. The effect of DBPT on pro-angiogenic molecules was analyzed by Western blotting and by an enzyme-linked immunosorbent assay.

resultsDBPT inhibited the growth of LNCaP and DU145 cells with 50% inhibitory concentrations ranging from 1.6 to 5.9 microM. Treating LNCaP and DU145 cells with DBPT led to a time-dependent cell-cycle arrest in the G(2)/M phase and increased levels of G(2)/M checkpoint proteins, such as cyclin B1, cdc25C, phosphorylated histone H(3), and MPM-2. DBPT induced the phosphorylation of Bcl-xL and Bim, and induced apoptosis, as evidenced by cleavage of caspase and poly (ADP-ribose) polymerase. DBPT also effectively induced apoptosis in Bcl-2-overexpressing DU145 cells. Furthermore, DBPT decreased hypoxia-inducible factor 1 alpha and vascular endothelial growth factor expression in LNCaP cells under both normoxia and hypoxia.

conclusionsDBPT can suppress proliferation, induce apoptosis, and down regulate pro-angiogenic molecules in prostate cancer cells, and might be useful in treating prostate cancer.

Indexed as

Neovascularization, PathologicApoptosisBlotting, WesternCell CycleCell ProliferationDown-RegulationEnzyme-Linked Immunosorbent AssayFlow CytometryHumansMalePhosphorylationProstatic NeoplasmsThiazolesThiazolidinesTumor Cells, Cultured5-(2,4-dihydroxybenzylidene)-2-(phenylimino)-1,3-thiazolidinThiazolesThiazolidines

Identifiers

PMID16302260
PMCPMC1351358

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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.