Evidence map›Paper›PMID 29117940›Full record

ArticleMolecular cancer research : MCR2018

ETV4 Facilitates Cell-Cycle Progression in Pancreatic Cells through Transcriptional Regulation of Cyclin D1.

Nikhil Tyagi, Sachin K Deshmukh, Sanjeev K Srivastava, Shafquat Azim, Aamir Ahmad, Ahmed Al-Ghadhban, Ajay P Singh, James E Carter, Bin Wang, Seema Singh

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer research : MCR, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.3field-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

32 citing papers in PubMed, 52 citations in OpenAlex.

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  8. Tissue-Specific Expression of the PorcineAnimals : an open access journal from MDPI · 2025
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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

10 authors at 2 institutions in 1 country.

Nikhil Tyagi *Department of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama.
Sachin K Deshmukh *Department of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama.
Sanjeev K SrivastavaDepartment of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama.
Shafquat AzimDepartment of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama.
Aamir AhmadDepartment of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama.
Ahmed Al-GhadhbanDepartment of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama.
Ajay P SinghDepartment of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama.
James E CarterDepartment of Pathology, College of Medicine, University of South Alabama, Mobile, Alabama.
Bin WangDepartment of Mathematics and Statistics, University of South Alabama, Mobile, Alabama.
Seema SinghDepartment of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama. seemasingh@health.southalabama.edu.
USA Mitchell Cancer Institute · USUniversity of South Alabama · US

Funding

Impact of social factors on breast cancer biology in African-American womenR01CA231925 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SINGH, SEEMA · 2019 to 2023
$3.0M
Targeting tumor-stromal interaction for pancreatic cancer therapyR01CA175772 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SINGH, AJAY PRATAP · 2014 to 2018
$1.9M
ETV4 in pancreatic cancerR03CA169829 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SINGH, SEEMA · 2012 to 2013
$144k
NCI NIH HHS R01 CA175772NCI NIH HHS R03 CA169829
6 · The paper itself

Abstract

The ETS family transcription factor ETV4 is aberrantly expressed in a variety of human tumors and plays an important role in carcinogenesis through upregulation of relevant target gene expression. Here, it is demonstrated that ETV4 is overexpressed in pancreatic cancer tissues as compared with the normal pancreas, and is associated with enhanced growth and rapid cell-cycle progression of pancreatic cancer cells. ETV4 expression was silenced through stable expression of a specific short hairpin RNA (shRNA) in two pancreatic cancer cell lines (ASPC1 and Colo357), while it was ectopically expressed in BXPC3 cells. Silencing of ETV4 in ASPC1 and Colo357 cells reduced the growth by 55.3% and 38.9%, respectively, while forced expression of ETV4 in BXPC3 cells increased the growth by 46.8% in comparison with respective control cells. Furthermore, ETV4-induced cell growth was facilitated by rapid transition of cells from G

Indexed as

Adenovirus E1A ProteinsCell CycleCell Line, TumorCell ProliferationCyclin D1Gene Expression ProfilingGene Expression Regulation, NeoplasticGene SilencingHumansPancreatic NeoplasmsPromoter Regions, GeneticProto-Oncogene ProteinsProto-Oncogene Proteins c-etsTranscription, GeneticUp-RegulationAdenovirus E1A ProteinsCCND1 protein, humanCyclin D1ETV4 protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins c-ets

Identifiers

PMID29117940
PMCPMC5805611
OpenAlexW2767263313

What OpenQuestion holds

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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.