Evidence map›Paper›PMID 27212033›Full record

ArticleOncogene2017

An important role for Myb-MuvB and its target gene KIF23 in a mouse model of lung adenocarcinoma.

F Iltzsche, K Simon, S Stopp, G Pattschull, S Francke, P Wolter, S Hauser, D J Murphy, P Garcia, A Rosenwald and 1 more

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed, 67 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 4 institutions in 2 countries.

F IltzscheDepartment of Physiological Chemistry, Biocenter, Theodor Boveri Institute, University of Wuerzburg, Wuerzburg, Germany.
K SimonDepartment of Physiological Chemistry, Biocenter, Theodor Boveri Institute, University of Wuerzburg, Wuerzburg, Germany.
S StoppDepartment of Physiological Chemistry, Biocenter, Theodor Boveri Institute, University of Wuerzburg, Wuerzburg, Germany.
G PattschullDepartment of Physiological Chemistry, Biocenter, Theodor Boveri Institute, University of Wuerzburg, Wuerzburg, Germany.
S FranckeDepartment of Physiological Chemistry, Biocenter, Theodor Boveri Institute, University of Wuerzburg, Wuerzburg, Germany.
P WolterDepartment of Physiological Chemistry, Biocenter, Theodor Boveri Institute, University of Wuerzburg, Wuerzburg, Germany.
S HauserDepartment of Physiological Chemistry, Biocenter, Theodor Boveri Institute, University of Wuerzburg, Wuerzburg, Germany.
D J MurphyInstitute of Cancer Sciences, University of Glasgow, and the CRUK Beatson Institute, Glasgow, UK.
P GarciaInstitute of Biomedical Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK.
A RosenwaldComprehensive Cancer Center Mainfranken, University of Wuerzburg, Wuerzburg, Germany.
S GaubatzDepartment of Physiological Chemistry, Biocenter, Theodor Boveri Institute, University of Wuerzburg, Wuerzburg, Germany.
University of Würzburg · DEComprehensive Cancer Center Mainfranken · DEUniversity of Birmingham · GBUniversity of Glasgow · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The conserved Myb-MuvB (MMB) multiprotein complex has an important role in transcriptional activation of mitotic genes. MMB target genes are overexpressed in several different cancer types and their elevated expression is associated with an advanced tumor state and a poor prognosis. This suggests that MMB could contribute to tumorigenesis by mediating overexpression of mitotic genes. However, although MMB has been extensively characterized biochemically, the requirement for MMB in tumorigenesis in vivo has not been investigated. Here we demonstrate that MMB is required for tumor formation in a mouse model of lung cancer driven by oncogenic K-RAS. We also identify a requirement for the mitotic kinesin KIF23, a key target gene of MMB, in tumorigenesis. RNA interference-mediated depletion of KIF23 inhibited lung tumor formation in vivo and induced apoptosis in lung cancer cell lines. Our results suggest that inhibition of KIF23 could be a strategy for treatment of lung cancer.

Indexed as

AdenocarcinomaAdenocarcinoma of LungAnimalsCell Line, TumorCell ProliferationCell Transformation, NeoplasticDisease Models, AnimalFemaleGene Expression Regulation, NeoplasticHeterograftsKinesinsLung NeoplasmsMaleMiceMice, KnockoutMitosisKinesinsMKLP1 protein, mouseMultiprotein ComplexesProto-Oncogene Proteins c-myb

Identifiers

PMID27212033
OpenAlexW2397003243

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.