Evidence map›Paper›PMID 22564737›Full record

ArticleBiochemical and biophysical research communications2012

Increased expression of bHLH transcription factor E2A (TCF3) in prostate cancer promotes proliferation and confers resistance to doxorubicin induced apoptosis.

Divya Patel, Jaideep Chaudhary

Abstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 51 citations in OpenAlex.

  1. BioMed research international · 2021
    Trial
  2. miR-138-5p inhibits WiT-49 cell growth in vitro by downregulating TCF3 expression, and suppresses tumorigenesis in vivo.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  11. RNAi-mediatedBioscience reports · 2017
    Article
  12. Expression of E2A in mid-secretory endometrium of women suffering from recurrent miscarriage.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2017
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  16. Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  17. ID4 promotes AR expression and blocks tumorigenicity of PC3 prostate cancer cells.Biochemical and biophysical research communications · 2016
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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

2 authors at 2 institutions in 1 country.

Divya PatelCenter for Cancer Research and Therapeutics Development, Clark Atlanta University, 223 James P. Brawley Dr. SW, Atlanta, GA 30314, USA.
Jaideep Chaudhary
Center for Cancer Research · USClark Atlanta University · US

Funding

THEORY OF PLANNED BEHAVIOR VS ETHNICITY /PHYSICAL ACTIVIG12RR003062 · NCRR · CLARK ATLANTA UNIVERSITY · PI BROWN, CARLTON B · 1985 to 2011
$15.5M
Inhibitor of Differentiation Gene Expression and Function in Prostate CellsR01CA128914 · NCI · CLARK ATLANTA UNIVERSITY · PI CHAUDHARY, JAIDEEP · 2009 to 2013
$1.4M
NCI NIH HHS CA128914NCI NIH HHS R01 CA128914NCRR NIH HHS G12 RR003062NCRR NIH HHS G12RR03062
6 · The paper itself

Abstract

E2A (TCF3) is a multifunctional basic helix loop helix (bHLH), transcription factor. E2A regulates transcription of target genes by homo- or heterodimerization with cell specific bHLH proteins. In general, E2A promotes cell differentiation, acts as a negative regulator of cell proliferation in normal cells and cancer cell lines and is required for normal B-cell development. Given the diverse biological pathways regulated/influenced by E2A little is known about its expression in cancer. In this study we investigated the expression of E2A in prostate cancer. Unexpectedly, E2A immuno-histochemistry demonstrated increased E2A expression in prostate cancer as compared to normal prostate. Silencing of E2A in prostate cancer cells DU145 and PC3 led to a significant reduction in proliferation due to G1 arrest that was in part mediated by increased CDKN1A(p21) and decreased Id1, Id3 and c-myc. E2A silencing in prostate cancer cell lines also resulted in increased apoptosis due to increased mitochondrial permeability and caspase 3/7 activation. Moreover, silencing of E2A increased sensitivity to doxorubicin induced apoptosis. Based on our results, we propose that E2A could be an upstream regulator of Id1 and c-Myc which are highly expressed in prostate cancer. These results for the first time demonstrate that E2A could in fact acts as a tumor promoter at least in prostate cancer.

Indexed as

ApoptosisDrug Resistance, NeoplasmAntibiotics, AntineoplasticBasic Helix-Loop-Helix ProteinsCell Line, TumorCell ProliferationDoxorubicinGene SilencingHumansMaleProstatic NeoplasmsAntibiotics, AntineoplasticBasic Helix-Loop-Helix ProteinsDoxorubicinTFPT protein, human

Identifiers

PMID22564737
PMCPMC3361642
OpenAlexW1998341518

What OpenQuestion holds

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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.