The integrative bioinformatic analysis deciphers the predicted molecular target gene and pathway from curcumin derivative CCA-1.1 against triple-negative breast cancer (TNBC).
Bioinformatics
CCA-1.1
Cell cycle
Mitosis
TNBC
Journal
Journal of the Egyptian National Cancer Institute
ISSN: 2589-0409
Titre abrégé: J Egypt Natl Canc Inst
Pays: England
ID NLM: 9424566
Informations de publication
Date de publication:
02 Aug 2021
02 Aug 2021
Historique:
received:
23
06
2021
accepted:
16
07
2021
entrez:
2
8
2021
pubmed:
3
8
2021
medline:
19
8
2021
Statut:
epublish
Résumé
The poor outcomes from triple-negative breast cancer (TNBC) therapy are mainly because of TNBC cells' heterogeneity, and chemotherapy is the current approach in TNBC treatment. A previous study reported that CCA-1.1, the alcohol-derivative from monocarbonyl PGV-1, exhibits anticancer activities against several cancer cells, as well as in TNBC. This time, we utilized an integrative bioinformatics approach to identify potential biomarkers and molecular mechanisms of CCA-1.1 in inhibiting proliferation in TNBC cells. Genomics data expression were collected through UALCAN, derived initially from TCGA-BRCA data, and selected for TNBC-only cases. We predict CCA-1.1 potential targets using SMILES-based similarity functions across six public web tools (BindingDB, DINIES, Swiss Target Prediction, Polypharmacology browser/PPB, Similarity Ensemble Approach/SEA, and TargetNet). The overlapping genes between the CCA-1.1 target and TNBC (CPTGs) were selected and used in further assessment. Gene ontology (GO) enrichment and the Kyoto Encyclopedia of Genes and Genomes (KEGG) network analysis were generated in WebGestalt. The protein-protein interaction (PPI) network was established in STRING-DB, and then the hub-genes were defined through Cytoscape. The hub-gene's survival analysis was processed via CTGS web tools using TCGA database. KEGG pathway analysis pointed to cell cycle process which enriched in CCA-1.1 potential targets. We also identified nine CPTGs that are responsible in mitosis, including AURKB, PLK1, CDK1, TPX2, AURKA, KIF11, CDC7, CHEK1, and CDC25B. We suggested CCA-1.1 possibly regulated cell cycle process during mitosis, which led to cell death. These findings needed to be investigated through experimental studies to reinforce scientific data of CCA-1.1 therapy against TNBC.
Sections du résumé
BACKGROUND
BACKGROUND
The poor outcomes from triple-negative breast cancer (TNBC) therapy are mainly because of TNBC cells' heterogeneity, and chemotherapy is the current approach in TNBC treatment. A previous study reported that CCA-1.1, the alcohol-derivative from monocarbonyl PGV-1, exhibits anticancer activities against several cancer cells, as well as in TNBC. This time, we utilized an integrative bioinformatics approach to identify potential biomarkers and molecular mechanisms of CCA-1.1 in inhibiting proliferation in TNBC cells.
METHODS
METHODS
Genomics data expression were collected through UALCAN, derived initially from TCGA-BRCA data, and selected for TNBC-only cases. We predict CCA-1.1 potential targets using SMILES-based similarity functions across six public web tools (BindingDB, DINIES, Swiss Target Prediction, Polypharmacology browser/PPB, Similarity Ensemble Approach/SEA, and TargetNet). The overlapping genes between the CCA-1.1 target and TNBC (CPTGs) were selected and used in further assessment. Gene ontology (GO) enrichment and the Kyoto Encyclopedia of Genes and Genomes (KEGG) network analysis were generated in WebGestalt. The protein-protein interaction (PPI) network was established in STRING-DB, and then the hub-genes were defined through Cytoscape. The hub-gene's survival analysis was processed via CTGS web tools using TCGA database.
RESULTS
RESULTS
KEGG pathway analysis pointed to cell cycle process which enriched in CCA-1.1 potential targets. We also identified nine CPTGs that are responsible in mitosis, including AURKB, PLK1, CDK1, TPX2, AURKA, KIF11, CDC7, CHEK1, and CDC25B.
CONCLUSION
CONCLUSIONS
We suggested CCA-1.1 possibly regulated cell cycle process during mitosis, which led to cell death. These findings needed to be investigated through experimental studies to reinforce scientific data of CCA-1.1 therapy against TNBC.
Identifiants
pubmed: 34337682
doi: 10.1186/s43046-021-00077-1
pii: 10.1186/s43046-021-00077-1
doi:
Substances chimiques
Cell Cycle Proteins
0
CDC7 protein, human
EC 2.7.1.-
Protein Serine-Threonine Kinases
EC 2.7.11.1
Curcumin
IT942ZTH98
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
19Informations de copyright
© 2021. The Author(s).
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