Evidence map›Paper›PMID 16024641›Full record

ArticleCancer research2005

Identification of a novel synthetic thiazolidin compound capable of inducing c-Jun NH2-terminal kinase-dependent apoptosis in human colon cancer cells.

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

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2005. 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
3.2field-weighted citation impact, top 9% 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, 43 citations in OpenAlex.

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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 1 institution in 1 country.

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

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Kathrin Milbury · 1985 to 2026
$290.8M
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
NCI NIH HHS CA16672NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA08582-01A1NCI NIH HHS R01 CA092487NCI NIH HHS R01 CA092487-01A1NCI NIH HHS R01 CA098582
6 · The paper itself

Abstract

Development of new therapeutic agents for colon cancer is highly desirable. To this end, we screened a chemical library for new anticancer agents and identified a synthetic compound, 5-(2,4-dihydroxybenzylidene)-2-(phenylimino)-1,3-thiazolidin (DBPT), which kills cancer cells more effectively than it kills normal human fibroblasts. The molecular mechanism of the antitumor action of DBPT was further analyzed in three human colorectal cancer cell lines. DBPT effectively inhibited the growth of colorectal cancer cells, independent of p53 and P-glycoprotein status, whereas normal fibroblasts were unaffected at the same IC50. Over time, DLD-1 cancer cells treated with DBPT underwent apoptosis. The general caspase inhibitor benzyloxycarbonyl-valine-alanine-aspartate-fluoromethylketone partially blocked DBPT-induced apoptosis in a dose-dependent manner. DBPT-induced apoptosis, including cytochrome c release and caspase activation, was abrogated when c-Jun NH2-terminal kinase (JNK) activation was blocked with either a specific JNK inhibitor or a dominant-negative JNK1 gene. However, constitutive JNK activation alone did not replicate the effects of DBPT in DLD-1 cells, and excessive JNK activation by adenovirus encoding MKK7 had little influence on DBPT-induced apoptosis. Our results suggested that DBPT induces apoptosis in colorectal cancer cell lines through caspase-dependent and caspase-independent pathways and that JNK activation was crucial for DBPT-induced apoptosis. DBPT and its analogues might be useful as anticancer agents.

Indexed as

AnthracenesApoptosisCaspasesCell Growth ProcessesCell Line, TumorColonic NeoplasmsEnzyme ActivationHCT116 CellsHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Signaling SystemThiazolesThiazolidines5-(2,4-dihydroxybenzylidene)-2-(phenylimino)-1,3-thiazolidinAnthracenesCaspasesJNK Mitogen-Activated Protein KinasespyrazolanthroneThiazolesThiazolidines

Identifiers

PMID16024641
PMCPMC1592468
OpenAlexW1967816930

What OpenQuestion holds

Textmetadata
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.