Evidence map›Paper›PMID 22222635›Full record

ArticleModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc2012

Overexpression and oncogenic function of aldo-keto reductase family 1B10 (AKR1B10) in pancreatic carcinoma.

Yeon Tae Chung, Kristina A Matkowskyj, Haonan Li, Han Bai, Wanying Zhang, Ming-Sound Tsao, Jie Liao, Guang-Yu Yang

Open access · bronzeAbstract read
In one paragraph

Article in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

71 citing papers in PubMed, 127 citations in OpenAlex.

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11 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 2 countries.

Yeon Tae ChungDepartment of Pathology, Northwestern University, Feinberg School of Medicine, Chicago, IL, USA.
Kristina A Matkowskyj
Haonan Li
Han Bai
Wanying Zhang
Ming-Sound Tsao
Jie Liao
Guang-Yu Yang
Northwestern University · USOntario Institute for Cancer Research · CA

Funding

Soluble epoxide hydrolase as a novel target of colitis-induced carcinogenesisR01CA137467 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI YANG, GUANG-YU · 2009 to 2012
$1.2M
Ulcerative colitis-associated cancer and its preventionR01CA104741 · NCI · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI YANG, GUANG-YU · 2004 to 2008
$1.2M
HMG-CoA reductase inhibitor, tea polyphenols and pancreatic cancer preventionR21CA122514 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI YANG, GUANG-YU · 2007 to 2008
$332k
NCI NIH HHS CA122514NCI NIH HHS CA137467NCI NIH HHS R01 CA104741NCI NIH HHS R01 CA137467NCI NIH HHS R21 CA122514
6 · The paper itself

Abstract

Aldo-keto reductase family 1B10 (AKR1B10) exhibits more restricted lipid substrate specificity (including farnesal, geranylgeranial, retinal and carbonyls), and metabolizing these lipid substrates has a crucial role in promoting carcinogenesis. Overexpression of AKR1B10 has been identified in smoking-related carcinomas such as lung cancer. As development of pancreatic cancer is firmly linked to smoking, the aim of the present study was to examine the expression and oncogenic role of AKR1B10 in pancreatic adenocarcinoma. AKR1B10 expression was analyzed in 50 paraffin-embedded clinical pancreatic cancer samples using immunohistochemistry. Oncogenic function of AKR1B10 was examined in pancreatic carcinoma cells in vitro using western blotting and siRNA approaches, mainly on cell apoptosis and protein prenylation including KRAS protein and its downstream signals. Immunohistochemistry analysis revealed that AKR1B10 overexpressed in 70% (35/50) of pancreatic adenocarcinomas and majority of pancreatic intraepithelial neoplasia, but not in adjacent morphologically normal pancreatic tissue. Compared with a normal pancreatic ductal epithelial cell (HPDE6E7), all of the six cultured pancreatic adenocarcinoma cell lines had an overexpression of AKR1B10 using immunoblotting, which correlated with increase of enzyme activity. siRNA-mediated silencing of AKR1B10 expression in pancreatic cancer cells resulted in (1) increased cell apoptosis, (2) increased non-farnesyled HDJ2 protein and (3) decreased membrane-bound prenylated KRAS protein and its downstream signaling molecules including phosphorylated ERK and MEK and membrane-bound E-cadherin. Our findings provide first time evidence that AKR1B10 is a unique enzyme involved in pancreatic carcinogenesis possibly via modulation of cell apoptosis and protein prenylation.

Indexed as

Gene Expression Regulation, NeoplasticAdenocarcinomaAldehyde ReductaseAldo-Keto ReductasesApoptosisBiomarkers, TumorCarcinoma in SituCell Line, TumorGene Knockdown TechniquesGene SilencingHSP40 Heat-Shock ProteinsHumansImmunohistochemistryPancreatic NeoplasmsProtein PrenylationAKR1B10 protein, humanAldehyde ReductaseAldo-Keto ReductasesBiomarkers, TumorDNAJA1 protein, humanHSP40 Heat-Shock Proteins

Identifiers

PMID22222635
PMCPMC3323665
OpenAlexW2014251969

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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.