Mapping of TP53 protein network using Cytoscape software

TP53 acts as a tumor suppressor in cancer. It induces cell cycle arrest or apoptosis in response to cellularstress and damage. p53 gene alteration could cause uncontrolled cell proliferation. In the present study, weused TP53 gene as the seed in the construction of a protein-protein interaction netw...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Pharmaceutical and biomedical research 2019-03
Hauptverfasser: Elengoe, Asita, Hamdan, Salehhuddin
Format: Artikel
Sprache:eng
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:TP53 acts as a tumor suppressor in cancer. It induces cell cycle arrest or apoptosis in response to cellularstress and damage. p53 gene alteration could cause uncontrolled cell proliferation. In the present study, weused TP53 gene as the seed in the construction of a protein-protein interaction network to identify genesthat might involve in tumorgenesis process with TP53. TP53 protein interaction database was obtainedfrom STRING version 9.1 program. High-throughput experimental data, literature data and hypotheticalstudies have been used to determine the roles of candidate genes in TP53 pathway. A total 500 genes fromSTRING database loaded into Cytoscape version 2.8.3. The 1762 protein interactions were assembled andvisualized in y organic form. We found eight specific non-overlapping clusters of various sizes, whichemerged from the huge network of protein-interactors using MCODE version 1.32 clustering algorithm.Biological Networks Gene Ontology (BiNGO) was used to determine two ontologies (molecular function andbiological process) involved in the protein network. Most of the genes mainly participated in gene andprotein expression, cell signaling and metabolism. A better understanding of the relationship between thegenes could aid in developing prognostic markers and better therapeutic strategies in cancer treatment.
ISSN:2423-4486
2423-4494
DOI:10.18502/pbr.v4i3.539