Evidence map›Paper›PMID 32495257›Full record

ArticleDigestive diseases and sciences2021

Integrin-Linked-Kinase Overexpression Is Implicated in Mechanisms of Genomic Instability in Human Colorectal Cancer.

Panagiota Chadla, Marina Arbi, Sofia Nikou, Theodoros Kalliakoudas, Helen Papadaki, Stavros Taraviras, Zoi Lygerou, Vasiliki Bravou

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Article in Digestive diseases and sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Integrin-linked kinase (ILK): the known vs. the unknown and perspectives.Cellular and molecular life sciences : CMLS · 2022
    Review
  5. 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

8 authors at 1 institution in 1 country.

Panagiota ChadlaDepartment of Anatomy, Histology and Embryology, Medical School, University of Patras, Rio, 26500, Greece.
Marina ArbiDepartment of Biology, Medical School, University of Patras, Rio, Greece.
Sofia NikouDepartment of Anatomy, Histology and Embryology, Medical School, University of Patras, Rio, 26500, Greece.
Theodoros KalliakoudasDepartment of Physiology, Medical School, University of Patras, Rio, Greece.
Helen PapadakiDepartment of Anatomy, Histology and Embryology, Medical School, University of Patras, Rio, 26500, Greece.
Stavros TaravirasDepartment of Physiology, Medical School, University of Patras, Rio, Greece.
Zoi LygerouDepartment of Biology, Medical School, University of Patras, Rio, Greece.
Vasiliki BravouDepartment of Anatomy, Histology and Embryology, Medical School, University of Patras, Rio, 26500, Greece. vibra@upatras.gr.ORCID 0000-0002-4635-0204
University of Patras · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGenomic instability is a hallmark of cancer cells contributing to tumor development and progression. Integrin-linked kinase (ILK) is a focal adhesion protein with well-established role in carcinogenesis. We have previously shown that ILK overexpression is critically implicated in human colorectal cancer (CRC) progression. In light of the recent findings that ILK regulates centrosomes and mitotic spindle formation, we aimed to determine its implication in mechanisms of genomic instability in human CRC.

methodsAssociation of ILK expression with markers of genomic instability (micronuclei formation, nucleus size, and intensity) was investigated in diploid human colon cancer cells HCT116 upon ectopic ILK overexpression, by immunofluorescence and in human CRC samples by Feulgen staining. We also evaluated the role of ILK in mitotic spindle formation, by immunofluorescence, in HCT116 cells upon inhibition and overexpression of ILK. Finally, we evaluated association of ILK overexpression with markers of DNA damage (p-H2AX, p-ATM/ATR) in human CRC tissue samples by immunohistochemistry and in ILK-overexpressing cells by immunofluorescence.

resultsWe showed that ILK overexpression is associated with genomic instability markers in human colon cancer cells and tissues samples. Aberrant mitotic spindles were observed in cells treated with specific ILK inhibitor (QLT0267), while ILK-overexpressing cells failed to undergo nocodazole-induced mitotic arrest. ILK overexpression was also associated with markers of DNA damage in HCT116 cells and human CRC tissue samples.

conclusionsThe above findings indicate that overexpression of ILK is implicated in mechanisms of genomic instability in CRC suggesting a novel role of this protein in cancer.

Indexed as

DNA DamageGenomic InstabilityMicronuclei, Chromosome-DefectiveAtaxia Telangiectasia Mutated ProteinsColorectal NeoplasmsHCT116 CellsHistonesHumansPhosphorylationProtein Serine-Threonine KinasesScaffold Protein ILKSignal TransductionSpindle ApparatusAtaxia Telangiectasia Mutated ProteinsATM protein, humanATR protein, humanH2AX protein, humanHistonesProtein Serine-Threonine KinasesScaffold Protein ILKColorectal cancerDNA damage responseGenomic instabilityILKMitosisReplication stress

Identifiers

PMID32495257
OpenAlexW3031993999

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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.