Evidence map›Paper›PMID 22977192›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2012

Overexpression of ecdysoneless in pancreatic cancer and its role in oncogenesis by regulating glycolysis.

Parama Dey, Satyanarayana Rachagani, Subhankar Chakraborty, Pankaj K Singh, Xiangshan Zhao, Channabasavaiah Basavaraju Gurumurthy, Judy M Anderson, Subodh Lele, Michael A Hollingsworth, Vimla Band and 1 more

Open access · greenAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

29 citing papers in PubMed, 40 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

11 authors at 2 institutions in 2 countries.

Parama DeyDepartment of Biochemistry and Molecular Biology, Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska 68198, USA.
Satyanarayana Rachagani
Subhankar Chakraborty
Pankaj K Singh
Xiangshan Zhao
Channabasavaiah Basavaraju Gurumurthy
Judy M Anderson
Subodh Lele
Michael A Hollingsworth
Vimla Band
Surinder K Batra
University of Nebraska Medical Center · USInstitute of Developmental Physiology · RU

Funding

UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Apar Kishor Ganti · 1985 to 2026
$55.0M
Tissue CoreP50CA127297 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI HOLLINGSWORTH, MICHAEL A. · 2008 to 2018
$17.1M
Early Diagnosis of Pancreatic CancerU01CA111294 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BATRA, SURINDER K., HOLLINGSWORTH, MICHAEL A. · 2004 to 2015
$7.1M
Role of N-Cadherin in Pancreatic Tumor MicroenvironmentU54CA163120 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BATRA, SURINDER K. · 2011 to 2015
$4.2M
A novel regulator of p53 functionR01CA096844 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAND, VIMLA · 2002 to 2011
$2.7M
Ecd as a regulator of cell cycle and breast oncogenesisR01CA144027 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BAND, VIMLA · 2011 to 2015
$1.6M
NCI NIH HHS CA144027NCI NIH HHS CA96844NCI NIH HHS P30 CA036727NCI NIH HHS P50 CA127297NCI NIH HHS R01 CA096844NCI NIH HHS R01 CA144027NCI NIH HHS SPORE P50CA127297NCI NIH HHS U01 CA111294NCI NIH HHS U54 CA163120NCI NIH HHS UO1CA11294PHS HHS U54163120
6 · The paper itself

Abstract

purposeTo study the expression and function of a novel cell-cycle regulatory protein, human ecdysoneless (Ecd), during pancreatic cancer pathogenesis. EXPERIMENTAL

designImmunohistochemical expression profiling of Ecd was done in nonneoplastic normal pancreatic tissues and pancreatic ductal adenocarcinoma lesions (from tissue microarray and Rapid Autopsy program) as well as precancerous PanIN lesions and metastatic organs. To analyze the biological significance of Ecd in pancreatic cancer progression, Ecd was stably knocked down in pancreatic cancer cell line followed by in vitro and in vivo functional assays.

resultsNormal pancreatic ducts showed very weak to no Ecd expression compared to significant positive expression in pancreatic cancer tissues (mean ± SE composite score: 0.3 ± 0.2 and 3.8 ± 0.2 respectively, P < 0.0001) as well as in PanIN precursor lesions with a progressive increase in Ecd expression with increasing dysplasia (PanIN-1-PanIN-3). Analysis of matched primary tumors and metastases from patients with pancreatic cancer revealed that Ecd is highly expressed in both primary pancreatic tumor and in distant metastatic sites. Furthermore, knockdown of Ecd suppressed cell proliferation in vitro and tumorigenicity of pancreatic cancer cells in mice orthotopic tumors. Microarray study revealed that Ecd regulates expression of glucose transporter GLUT4 in pancreatic cancer cells and was subsequently shown to modulate glucose uptake, lactate production, and ATP generation by pancreatic cancer cells. Finally, knockdown of Ecd also reduced level of pAkt, key signaling molecule known to regulate aerobic glycolysis in cancer cells.

conclusionEcd is a novel tumor-promoting factor that is differentially expressed in pancreatic cancer and potentially regulates glucose metabolism within cancer cells.

Indexed as

GlycolysisAnimalsCarcinoma, Pancreatic DuctalCarrier ProteinsCell ProliferationCell Transformation, NeoplasticFemaleGene ExpressionGene Expression Regulation, NeoplasticGlucoseGlucose Transporter Type 4HumansLymphatic MetastasisMiceMice, NudeNeoplasm TransplantationCarrier ProteinsECD protein, humanGlucoseGlucose Transporter Type 4SLC2A4 protein, human

Identifiers

PMID22977192
PMCPMC3551465
OpenAlexW2124211678

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Registered trials

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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.