Evidence map›Paper›PMID 34687379›Full record

ArticleMedical oncology (Northwood, London, England)2021

Enhancement of Apo2L/TRAIL signaling pathway receptors by the activation of Klotho gene with CRISPR/Cas9 in Caco-2 colon cancer cells.

Sibel Gunes, Merve Nur Soykan, Ayla Eker Sariboyaci, Onur Uysal, Tugba Semerci Sevimli

Abstract read
PubMed Publisher
In one paragraph

Article in Medical oncology (Northwood, London, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 11 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

5 authors at 1 institution in 1 country.

Sibel GunesCellular Therapy and Stem Cell Production Application and Research Centre, ESTEM, Eskisehir Osmangazi University, 26480, Eskisehir, Turkey. gunesibel@gmail.com.ORCID http://orcid.org/0000-0003-0846-1170
Merve Nur SoykanCellular Therapy and Stem Cell Production Application and Research Centre, ESTEM, Eskisehir Osmangazi University, 26480, Eskisehir, Turkey.ORCID http://orcid.org/0000-0003-1231-9791
Ayla Eker SariboyaciCellular Therapy and Stem Cell Production Application and Research Centre, ESTEM, Eskisehir Osmangazi University, 26480, Eskisehir, Turkey.ORCID http://orcid.org/0000-0003-4536-9859
Onur UysalCellular Therapy and Stem Cell Production Application and Research Centre, ESTEM, Eskisehir Osmangazi University, 26480, Eskisehir, Turkey.ORCID http://orcid.org/0000-0001-6800-5607
Tugba Semerci SevimliCellular Therapy and Stem Cell Production Application and Research Centre, ESTEM, Eskisehir Osmangazi University, 26480, Eskisehir, Turkey.ORCID http://orcid.org/0000-0003-4856-2304
Eskişehir Osmangazi University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human Klotho gene has many known functions such as anti-aging and anti-tumor, and decreased expression of this gene causes malignant formations in most types of cancer, including colon cancer. Interacting with TRAIL death receptors (DR4 and DR5) induces an apoptotic effect in cancer treatments by reducing the proliferation of cancer cells. The present study aimed to investigate downstream effect of overexpression of Klotho gene, which is known to have an antitumor effect on resistant human colon cancer cells, by examining its action on TRAIL death and decoy (DcR1 and DcR2) receptors for the first time. For this purpose, upregulation of human Klotho gene was achieved with CRISPR/Cas9-mediated system in resistant human colon cancer Caco-2 cells. To determine the effect of upregulation of Klotho gene on cancer cells evaluations with flow cytometry, WST-8, qRT-PCR, ELISA, and immunohistochemical analysis were performed. Then, Klotho gene was knocked out and its apoptotic effect was tested to find out whether it is due to overexpression of Klotho gene or not. Our results indicate that overexpression of Klotho gene in Caco-2 cells via CRISPR/Cas9-sensitized TRAIL death receptor DR4 suppresses the proliferation of cells by leading to apoptosis. Thus, this study conducted on apoptosis-resistant colon cancer cells may bring new insights about the role of Klotho gene in colon cancer.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisCaco-2 CellsColonic NeoplasmsCRISPR-Cas SystemsHumansKlotho ProteinsReceptors, TNF-Related Apoptosis-Inducing LigandSignal TransductionKlotho ProteinsKL protein, humanReceptors, TNF-Related Apoptosis-Inducing LigandCaco-2 cellsColon cancerCRISPR/Cas9KlothoTRAIL death receptor

Identifiers

PMID34687379
OpenAlexW3205304416

What OpenQuestion holds

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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.