Evidence map›Paper›PMID 24913355›Full record

ArticleMolecular cancer2014

Expression and Y435-phosphorylation of Abelson interactor 1 (Abi1) promotes tumour cell adhesion, extracellular matrix degradation and invasion by colorectal carcinoma cells.

Konrad Steinestel, Silke Brüderlein, Jochen K Lennerz, Julie Steinestel, Klaus Kraft, Christian Pröpper, Viktor Meineke, Peter Möller

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 34 citations in OpenAlex.

  1. Trial
  2. Adaptor protein Abelson interactor 1 in homeostasis and disease.Cell communication and signaling : CCS · 2024
    Review
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  7. ABI2-mediated MEOX2/KLF4-NANOG axis promotes liver cancer stem cell and drives tumour recurrence.Liver international : official journal of the International Association for the Study of the Liver · 2022
    Article
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  12. CRISPR/CAS9-mediated knockout of Abi1 inhibits p185Journal of hematology & oncology · 2020
    Article
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  16. 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

8 authors at 4 institutions in 1 country.

Konrad SteinestelBundeswehr Institute of Radiobiology, Neuherbergstr, 11, 80937 Munich, Germany. konrad@steinestel.com.
Silke Brüderlein
Jochen K Lennerz
Julie Steinestel
Klaus Kraft
Christian Pröpper
Viktor Meineke
Peter Möller
University Hospital Ulm · DEInstitut für Radiobiologie der BundeswehrBundeswehrkrankenhaus · DEUniversität Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe Abelson tyrosine kinase (c-Abl) inhibitor STI571 (Glivec®) has been shown to effectively inhibit colorectal cancer cell migration and invasion. The c-Abl substrate abelson interactor 1 (Abi1) is a key regulator of actin reorganization and upregulated in colorectal carcinoma. The specific role of Abi1 in relation to extracellular matrix degradation and effects of targeting Abi1 phosphorylation have not yet been examined. Here, we investigated the role of Abi1 in relation to invasive properties in colorectal cancer. METHODS AND

resultsIn 56 primary human colorectal carcinoma samples, we found overexpression of Abi1 in 39% at the invasive edge of the tumour, associated with an infiltrative phenotype and high-grade tumour cell budding (p = 0.001). To explore the role of Abi1 in vitro, we employed the Abi1 expressing and KRAS-mutated CHD1 model and performed matrix degradation assays that showed Abi1 localization at specific sites of matrix degradation. Moreover, quantification of matrix dissolution demonstrated suppression after RNAi knockdown of Abi1 by 95% (p = 0.001). Importantly, treatment with STI571 did abolish Abi1 Y435-phosphorylation, suppressed the matrix dissolution, decreased fibronectin attachment, and suppressed cell invasion through reconstituted extracellular matrix.

conclusionOur data indicate that phosphorylated Abi1 contributes to the invasive properties of colorectal cancer.

Indexed as

ActinsAdaptor Proteins, Signal TransducingAgedAged, 80 and overBenzamidesCell AdhesionCell MovementColorectal NeoplasmsCytoskeletal ProteinsDNA-Binding ProteinsDNA HelicasesExtracellular MatrixFemaleGene Expression Regulation, NeoplasticHumansImatinib MesylateABI1 protein, humanActinsAdaptor Proteins, Signal TransducingBenzamidesCHD1 protein, humanCytoskeletal ProteinsDNA-Binding ProteinsDNA HelicasesImatinib MesylateKRAS protein, humanPiperazinesProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)Pyrimidinesras Proteins

Identifiers

PMID24913355
PMCPMC4066275
OpenAlexW2124004452

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.