Evidence map›Paper›PMID 22808230›Full record

ArticlePloS one2012

Expression of Abelson interactor 1 (Abi1) correlates with inflammation, KRAS mutation and adenomatous change during colonic carcinogenesis.

Konrad Steinestel, Silke Brüderlein, Julie Steinestel, Bruno Märkl, Michael J Schwerer, Annette Arndt, Klaus Kraft, Christian Pröpper, Peter Möller

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Adaptor protein Abelson interactor 1 in homeostasis and disease.Cell communication and signaling : CCS · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Regulators of Actin Dynamics in Gastrointestinal Tract Tumors.Gastroenterology research and practice · 2015
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. 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

9 authors at 3 institutions in 1 country.

Konrad SteinestelInstitute of Pathology, University of Ulm, Ulm, Germany. konrad@steinestel.com
Silke Brüderlein
Julie Steinestel
Bruno Märkl
Michael J Schwerer
Annette Arndt
Klaus Kraft
Christian Pröpper
Peter Möller
Universität Ulm · DEBundeswehrkrankenhaus · DEUniversity Hospital Augsburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAbelson interactor 1 (Abi1) is an important regulator of actin dynamics during cytoskeletal reorganization. In this study, our aim was to investigate the expression of Abi1 in colonic mucosa with and without inflammation, colonic polyps, colorectal carcinomas (CRC) and metastases as well as in CRC cell lines with respect to BRAF/KRAS mutation status and to find out whether introduction of KRAS mutation or stimulation with TNFalpha enhances Abi1 protein expression in CRC cells. METHODOLOGY/PRINCIPAL

findingsWe immunohistochemically analyzed Abi1 protein expression in 126 tissue specimens from 95 patients and in 5 colorectal carcinoma cell lines with different mutation status by western immunoblotting. We found that Abi1 expression correlated positively with KRAS, but not BRAF mutation status in the examined tissue samples. Furthermore, Abi1 is overexpressed in inflammatory mucosa, sessile serrated polyps and adenomas, tubular adenomas, invasive CRC and CRC metastasis when compared to healthy mucosa and BRAF-mutated as well as KRAS wild-type hyperplastic polyps. Abi1 expression in carcinoma was independent of microsatellite stability of the tumor. Abi1 protein expression correlated with KRAS mutation in the analyzed CRC cell lines, and upregulation of Abi1 could be induced by TNFalpha treatment as well as transfection of wild-type CRC cells with mutant KRAS. The overexpression of Abi1 could be abolished by treatment with the PI3K-inhibitor Wortmannin after KRAS transfection. CONCLUSIONS/SIGNIFICANCE: Our results support a role for Abi1 as a downstream target of inflammatory response and adenomatous change as well as oncogenic KRAS mutation via PI3K, but not BRAF activation. Furthermore, they highlight a possible role for Abi1 as a marker for early KRAS mutation in hyperplastic polyps. Since the protein is a key player in actin dynamics, our data encourages further studies concerning the exact role of Abi1 in actin reorganization upon enhanced KRAS/PI3K signalling during colonic tumorigenesis.

Indexed as

Adaptor Proteins, Signal TransducingAdenomaAgedCell Line, TumorCell Transformation, NeoplasticColonic NeoplasmsCytoskeletal ProteinsFemaleHumansImmunohistochemistryInflammationIntestinal MucosaMaleMiddle AgedModels, BiologicalMutationABI1 protein, humanAdaptor Proteins, Signal TransducingBRAF protein, humanCytoskeletal ProteinsKRAS protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)ras ProteinsTumor Necrosis Factor-alpha

Identifiers

PMID22808230
PMCPMC3393686
OpenAlexW2009152960

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LicenceCC BY
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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.