Evidence map›Paper›PMID 38627442›Full record

ArticleScientific reports2024

New treatment alternatives for primary and metastatic colorectal cancer by an integrated transcriptome and network analyses.

Caner Karaca, Ezgi Demir Karaman, Asim Leblebici, Hasan Kurter, Hulya Ellidokuz, Altug Koc, Ender Berat Ellidokuz, Zerrin Isik, Yasemin Basbinar

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.7field-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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Article
  3. 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 1 institution in 1 country.

Caner Karaca *Department of Translational Oncology, Institute of Health Sciences, Dokuz Eylul University, Izmir, Turkey.
Ezgi Demir Karaman *Department of Computer Engineering, Faculty of Engineering, Dokuz Eylul University, Izmir, Turkey.
Asim LeblebiciDepartment of Translational Oncology, Institute of Health Sciences, Dokuz Eylul University, Izmir, Turkey.
Hasan KurterDepartment of Translational Oncology, Institute of Health Sciences, Dokuz Eylul University, Izmir, Turkey.
Hulya EllidokuzDepartment of Preventive Oncology, Institute of Oncology, Dokuz Eylul University, Izmir, Turkey.
Altug KocDepartment of Translational Oncology, Institute of Health Sciences, Dokuz Eylul University, Izmir, Turkey.
Ender Berat EllidokuzDepartment of Gastroenterology, Faculty of Medicine, Dokuz Eylul University, Izmir, Turkey.
Zerrin IsikDepartment of Computer Engineering, Faculty of Engineering, Dokuz Eylul University, Izmir, Turkey. zerrin@cs.deu.edu.tr.
Yasemin BasbinarDepartment of Translational Oncology, Institute of Oncology, Dokuz Eylul University, Izmir, Turkey. ybaskin65@gmail.com.
Dokuz Eylül University · TR

Funding

TUSEB Scientific Research Project Coordination Unit 2019.4079
6 · The paper itself

Abstract

Metastatic colorectal cancer (CRC) is still in need of effective treatments. This study applies a holistic approach to propose new targets for treatment of primary and liver metastatic CRC and investigates their therapeutic potential in-vitro. An integrative analysis of primary and metastatic CRC samples was implemented for alternative target and treatment proposals. Integrated microarray samples were grouped based on a co-expression network analysis. Significant gene modules correlated with primary CRC and metastatic phenotypes were identified. Network clustering and pathway enrichments were applied to gene modules to prioritize potential targets, which were shortlisted by independent validation. Finally, drug-target interaction search led to three agents for primary and liver metastatic CRC phenotypes. Hesperadin and BAY-1217389 suppress colony formation over a 14-day period, with Hesperadin showing additional efficacy in reducing cell viability within 48 h. As both candidates target the G2/M phase proteins NEK2 or TTK, we confirmed their anti-proliferative properties by Ki-67 staining. Hesperadinin particular arrested the cell cycle at the G2/M phase. IL-29A treatment reduced migration and invasion capacities of TGF-β induced metastatic cell lines. In addition, this anti-metastatic treatment attenuated TGF-β dependent mesenchymal transition. Network analysis suggests IL-29A induces the JAK/STAT pathway in a preventive manner.

Indexed as

Colonic NeoplasmsColorectal NeoplasmsIndolesLiver NeoplasmsRectal NeoplasmsSulfonamidesCell Line, TumorCell MovementGene Expression Regulation, NeoplasticHumansJanus KinasesNIMA-Related KinasesSignal TransductionSTAT Transcription FactorsTranscriptomeTransforming Growth Factor betahesperadinIndolesJanus KinasesNEK2 protein, humanNIMA-Related KinasesSTAT Transcription FactorsSulfonamidesTransforming Growth Factor beta

Identifiers

PMID38627442
PMCPMC11021540
OpenAlexW4394832217

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.