Evidence map›Paper›PMID 17019648›Full record

ArticleMammalian genome : official journal of the International Mammalian Genome Society2006

Intestinal overexpression of ZNF148 suppresses ApcMin/+ neoplasia.

David J Law, Edwin M Labut, Juanita L Merchant

Abstract read
PubMed Publisher
In one paragraph

Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

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  4. MRTFB suppresses colorectal cancer development through regulating SPDL1 and MCAM.Proceedings of the National Academy of Sciences of the United States of America · 2019
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  16. DNA copy-number alterations underlie gene expression differences between microsatellite stable and unstable colorectal cancers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2008
    Article
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

3 authors at 2 institutions in 1 country.

David J LawDepartment of Internal Medicine, University of Michigan, Ann Arbor, Michigan, 48109-2200, USA.
Edwin M Labut
Juanita L Merchant
University of Michigan–Ann Arbor · USMichigan Medicine · US

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THEODORE S LAWRENCE · 1988 to 2026
$178.2M
University of Michigan Center for Gastrointestinal ResearchP30DK034933 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI OWYANG, CHUNG · 1986 to 2021
$22.5M
Mechanisms of Gastrointestional Growth &TransformationR01DK055732 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MERCHANT, JUANITA L. · 2000 to 2014
$4.1M
Mechanisms of Gastrointestinal Growth and TransformationR56DK055732 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MERCHANT, JUANITA L. · 2010 to 2010
$369k
ZBP-89 isoforms in gastrointestinal diseasesR21DK065004 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LAW, DAVID J · 2003 to 2004
$298k
NCI NIH HHS 5P30CA46592NIDDK NIH HHS 2P30DK34933-20NIDDK NIH HHS DK065004NIDDK NIH HHS DK55732NIDDK NIH HHS P30 DK034933NIDDK NIH HHS R01 DK055732
6 · The paper itself

Abstract

ZNF148 (ZBP-89, Zfp148) is a multifunctional transcription factor expressed at low levels in most tissues. When overexpressed in gastrointestinal cancer cell lines, ZNF148 inhibits cellular proliferation and induces apoptosis. We sought to determine whether intestinal ZNF148 overexpression would abrogate adenoma development in the ApcMin/+ mouse, i.e., whether ZNF148 is a tumor suppressor. The 13-kb villin promoter was spliced upstream of the ZNF148 cDNA to generate transgenic villin-ZNF148 (ZNF148TgVZ) mice. Intestinal mucosal ZNF148 expression was elevated in four of five ZNF148(TgVZ) lineages and correlated with increased caspase-3 expression and activation. In addition, DNA fragmentation was increased in ZNF148TgVZ mice relative to wild-type littermates. These results suggested that increased intestinal ZNF148 expression induces apoptosis. ZNF148TgVZ mice were crossed with ApcMin/+ mice to assess the biological significance of intestinal ZNF148 overexpression. The presence of the ZNF148TgVZ allele in ApcMin/+ mice correlated with reduced gastrointestinal bleeding at 5 weeks, a 50% reduction in adenoma burden at 20-22 weeks, and prolonged survival (median survival of 33.5 days vs. 21.5 days), relative to nontransgenic littermates. These data suggest that enhanced ZNF148 expression activates intestinal apoptosis and thereby mitigates disease burden in ApcMin/+ mice. They also suggest that ZNF148 is a therapeutic target to inhibit colon cancer development.

Indexed as

AdenomaAdenomatous Polyposis Coli ProteinAllelesAnimalsApoptosisCrosses, GeneticDNA-Binding ProteinsGastrointestinal DiseasesHemorrhageIntestinal MucosaIntestinal NeoplasmsMiceMice, Inbred C57BLMice, TransgenicPedigreeSurvival AnalysisAdenomatous Polyposis Coli ProteinDNA-Binding ProteinsTranscription FactorsTumor Suppressor ProteinsZNF148 protein, human

Identifiers

PMID17019648
OpenAlexW2016398433

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.