Evidence map›Paper›PMID 33098056›Full record

ArticleDaru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences2020

Functional network analysis reveals potential repurposing of β-blocker atenolol for pancreatic cancer therapy.

Adam Hermawan, Herwandhani Putri, Rohmad Yudi Utomo

Open access · greenAbstract read
In one paragraph

Article in Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.1field-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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. β-Adrenoceptors in Cancer: Old Players and New Perspectives.Handbook of experimental pharmacology · 2024
    Review
  3. Review
  4. Review
  5. Article
  6. 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

3 authors at 1 institution in 1 country.

Adam HermawanLaboratory of Macromolecular Engineering, Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Universitas Gadjah Mada Sekip Utara II, Yogyakarta, 55281, Indonesia. adam_apt@ugm.ac.id.ORCID https://orcid.org/0000-0001-5851-3691
Herwandhani PutriCancer Chemoprevention Research Center, Faculty of Pharmacy, Universitas Gadjah Mada Sekip Utara II, Yogyakarta, 55281, Indonesia.ORCID https://orcid.org/0000-0002-6463-1771
Rohmad Yudi UtomoLaboratory of Medicinal Chemistry, Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Universitas Gadjah Mada Sekip Utara II, Yogyakarta, 55281, Indonesia.ORCID https://orcid.org/0000-0003-4803-9417
Universitas Gadjah Mada · ID

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe survival rate of patients with pancreatic cancer is low; therefore, continuous discovery and development of novel pancreatic cancer drugs are required. Functional network analysis is an integrated bioinformatics approach based on gene, target, and disease networks interaction, and it is extensively used in drug discovery and development.

objectiveThis study aimed to identify if atenolol, a selective adrenergic inhibitor, can be repurposed for the treatment of pancreatic cancer using functional network analysis.

methodsDirect target proteins (DTPs) and indirect target proteins (ITPs) were obtained from STITCH and STRING databases, respectively. Atenolol-mediated proteins (AMPs) were collected from DTPs and ITPs and further analyzed for gene ontology, KEGG pathway enrichment, genetic alterations, overall survival, and molecular docking.

resultsWe obtained 176 AMPs that consisted of 10 DTPs and 166 ITPs. Among the AMPs involved in the pancreatic cancer pathways, several AMPs such as MAPK1, RELA, MAPK8, STAT1, and STAT3 were identified. Genetic alterations in seven AMPs were identified in 0.9%-16% of patients. Patients with high mRNA levels of MAPK1, RELA, STAT3, GNB1, and MMP9 had significantly worse overall survival rates compared with patients with low expression. Molecular docking studies showed that RELA and MMP9 are potential target candidates of atenolol in the treatment of patients with pancreatic cancer.

conclusionIn conclusion, atenolol can potentially be repurposed to target pancreatic cancer cells by modulating MMP9 and NF-κB signaling. The results of this study need to be further validated in vitro and in vivo.

Indexed as

Up-RegulationAtenololDatabases, GeneticDrug RepositioningGene Expression Regulation, NeoplasticHumansKaplan-Meier EstimateMatrix Metalloproteinase 9Models, MolecularMolecular Docking SimulationPancreatic NeoplasmsSignal TransductionSurvival AnalysisTranscription Factor RelAAtenololMatrix Metalloproteinase 9MMP9 protein, humanRELA protein, humanTranscription Factor RelAAtenololDrug repurposingFunctional networkPancreatic cancer

Identifiers

PMID33098056
PMCPMC7704874
OpenAlexW3094321536

What Socratic holds

Textmetadata
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 Socratic graph.