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Updated: Aug 25, 2025
Performing Data Mining And Integrative Analysis Of Biomarker in Breast Cancer Using Multiple Publicly Accessible Databases
Published on: May 17, 2019
Microarray data reveal potential genes that regulate triple-negative breast cancer
Chi Pan1, Aihua Cong2, Qingtao Ni2
1Department of General Surgery, Jiangsu Taizhou People's Hospital, Taizhou, China.
Objective:
Triple-negative breast cancer (TNBC) is characterized by a lack of targeted therapies and poor patient prognosis, and its underlying pathological mechanisms remain unclear. This study aimed to identify potential key genes and related pathways that are required for TNBC development.
Methods:
We screened the Gene Expression Omnibus database for transcriptome data and identified differently expressed genes in TNBC. Then, we performed Gene Ontology analysis to determine the genes and pathways involved in TNBC development. We correlated significantly expressed genes and miRNAs using miRDB, TargetScan, miRWalk, and DIANA, and then validated the expression of CDK1 and miR-143-3p in TNBC patients.
Results:
Eighteen genes were significantly upregulated in TNBC patients, and these were found to be enriched in cell metabolic process, cell division, mitochondrion, and respiratory chain. MiR-143-3p was found to be an upstream regulator of CDK1. Validation experiments revealed that CDK1 was upregulated while miR-143-3p was downregulated in clinical TNBC specimens.
Conclusions:
Collectively, our results revealed 18 upregulated genes in TNBC. Notably, CDK1 and its related microRNA miR-143-3p could be potential therapeutic targets for TNBC.
Insights
Triple-negative breast cancer (TNBC) research identified 18 upregulated genes, including CDK1. MiR-143-3p, a regulator of CDK1, was downregulated, suggesting both could be therapeutic targets for TNBC.
Area of Science:
- Oncology
- Genomics
- Molecular Biology
Background:
- Triple-negative breast cancer (TNBC) presents significant challenges due to limited targeted therapies and poor prognoses.
- The precise pathological mechanisms driving TNBC development are not fully understood.
Purpose of the Study:
- To identify key genes and associated molecular pathways crucial for TNBC development.
- To uncover potential therapeutic targets for TNBC.
Main Methods:
- Screened Gene Expression Omnibus (GEO) database for transcriptome data to identify differentially expressed genes in TNBC.
- Utilized Gene Ontology analysis to pinpoint involved genes and pathways.
- Correlated gene and microRNA (miRNA) expression using multiple databases (miRDB, TargetScan, miRWalk, DIANA).
- Validated expression of Cyclin-Dependent Kinase 1 (CDK1) and miR-143-3p in clinical TNBC samples.
Main Results:
- Identified 18 significantly upregulated genes in TNBC, enriched in cell metabolism, division, mitochondria, and respiratory chain processes.
- Established miR-143-3p as an upstream regulator of CDK1.
- Clinical validation confirmed CDK1 upregulation and miR-143-3p downregulation in TNBC specimens.
Conclusions:
- The study identified 18 upregulated genes associated with TNBC.
- CDK1 and its regulatory miRNA, miR-143-3p, emerged as potential therapeutic targets for TNBC treatment.
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