Evidence map›Paper›PMID 15122344›Full record

ArticleOncogene2004

Induction of S-phase arrest and p21 overexpression by a small molecule 2[[3-(2,3-dichlorophenoxy)propyl] amino]ethanol in correlation with activation of ERK.

Hongbo Zhu, Lidong Zhang, Shuhong Wu, Fuminori Teraishi, John J Davis, Dietmar Jacob, Bingliang Fang

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

41 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
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  6. Non-ubiquitous expression of core spliceosomal protein SmB/B' in chick and mouse embryos.Developmental dynamics : an official publication of the American Association of Anatomists · 2023
    Article
  7. Article
  8. Article
  9. Dichloromethane fractions ofMolecular medicine reports · 2022
    Article
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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.

Hongbo ZhuDepartment of Thoracic and Cardiovascular Surgery, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Lidong Zhang
Shuhong Wu
Fuminori Teraishi
John J Davis
Dietmar Jacob
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 Scott Kopetz · 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 R01 CA 092487-01A1NCI NIH HHS R01 CA 098582-01A1
6 · The paper itself

Abstract

We recently found that a small molecule 2[[3-(2,3-dichlorophenoxy)propyl]amino]ethanol (2,3-DCPE) could induce apoptosis and downregulate Bcl-XL expression in various cancer cells. Here, we found that 2,3-DCPE suppressed the proliferation of Bcl-XL-overexpressing cancer cells without inducing apoptosis. Subsequently, we found that 2,3-DCPE could induce S-phase arrest and upregulate p21 but not p27 at a time- and dose-dependent but p53-dispensable manner in DLD-1 human colon cancer cells. Activation of ERK was also detected after treatment with 2,3-DCPE. Moreover, p21 induction was dramatically attenuated by ERK inhibitors PD98059 and U0126. Induction of p21 and S-phase arrest and corresponding activation of ERK were also observed in ATM-defective cells, suggesting that 2,3-DCPE-induced these events were ATM-dispensable. Furthermore, ERK inhibitors dramatically attenuated 2,3-DCPE-induced S-phase arrest. Together, our data indicate that ERK activation correlated with the 2,3-DCPE-mediated induction of p21 expression and S-phase arrest. This finding may have implication for cancer therapy.

Indexed as

S PhaseApoptosisAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell Line, TumorChlorobenzenesCyclin-Dependent Kinase Inhibitor p21CyclinsDNA-Binding ProteinsDown-RegulationEthanolaminesGene Expression Regulation, NeoplasticHumansMitogen-Activated Protein KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-bcl-22-((3-(2,3-dichlorophenoxy)propyl)amino)ethanolAtaxia Telangiectasia Mutated ProteinsATM protein, humanCDKN1A protein, humanCell Cycle ProteinsChlorobenzenesCyclin-Dependent Kinase Inhibitor p21CyclinsDNA-Binding ProteinsEthanolaminesMitogen-Activated Protein KinasesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-bcl-2Tumor Suppressor Protein p53Tumor Suppressor Proteins

Identifiers

PMID15122344
OpenAlexW1963730069

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.