Evidence map›Paper›PMID 23752186›Full record

ArticleOncogene2014

EVI1 oncogene promotes KRAS pathway through suppression of microRNA-96 in pancreatic carcinogenesis.

M Tanaka, H I Suzuki, J Shibahara, A Kunita, T Isagawa, A Yoshimi, M Kurokawa, K Miyazono, H Aburatani, S Ishikawa and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.0field-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

40 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Pancreatic Cancer: Genetic Conditions and Epigenetic Alterations.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2023
    Review
  6. Article
  7. Review
  8. Review
  9. International journal of molecular sciences · 2022
    Article
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  13. Review
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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 1 institution in 1 country.

M TanakaDepartment of Pathology, University of Tokyo, Tokyo, Japan.
H I SuzukiDepartment of Molecular Pathology, University of Tokyo, Tokyo, Japan.
J ShibaharaDepartment of Pathology, University of Tokyo, Tokyo, Japan.
A KunitaDepartment of Pathology, University of Tokyo, Tokyo, Japan.
T IsagawaDepartment of Cardiovascular Medicine, University of Tokyo, Tokyo, Japan.
A YoshimiDepartment of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
M KurokawaDepartment of Hematology and Oncology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
K MiyazonoDepartment of Molecular Pathology, University of Tokyo, Tokyo, Japan.
H AburataniGenome Science Division, RCAST, University of Tokyo, Tokyo, Japan.
S IshikawaDepartment of Pathology, University of Tokyo, Tokyo, Japan.
M FukayamaDepartment of Pathology, University of Tokyo, Tokyo, Japan.
The University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite frequent KRAS mutation, the early molecular mechanisms of pancreatic ductal adenocarcinoma (PDAC) development have not been fully elucidated. By tracking a potential regulator of another feature of PDAC precursors, acquisition of foregut or gastric epithelial gene signature, we herein report that aberrant overexpression of ecotropic viral integration site 1 (EVI1) oncoprotein, which is usually absent in normal pancreatic duct, is a widespread marker across the full spectrum of human PDAC precursors and PDAC. In pancreatic cancer cells, EVI1 depletion caused remarkable inhibition of cell growth and migration, indicating its oncogenic roles. Importantly, we found that EVI1 upregulated KRAS expression through suppression of a potent KRAS suppressor, miR-96, in pancreatic cancer cells. Collectively, the present findings suggest that EVI1 overexpression and KRAS mutation converge on activation of the KRAS pathway in early phases of pancreatic carcinogenesis and propose EVI1 and/or miR-96 as early markers and therapeutic targets in this dismal disease.

Indexed as

Blotting, WesternCarcinoma, Pancreatic DuctalCell Line, TumorChromatin ImmunoprecipitationDNA-Binding ProteinsGene Expression Regulation, NeoplasticHumansImmunohistochemistryMDS1 and EVI1 Complex Locus ProteinMicroRNAsMutationOligonucleotide Array Sequence AnalysisOncogenesPancreatic NeoplasmsProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)DNA-Binding ProteinsKRAS protein, humanMDS1 and EVI1 Complex Locus ProteinMECOM protein, humanMicroRNAsMIRN96 microRNA, humanProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)ras ProteinsRNA, Small InterferingTranscription Factors

Identifiers

PMID23752186
OpenAlexW2041336158

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.