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Bioinformatic analysis reveals MIR502 as a potential tumour suppressor in ovarian cancer
1Department of Obstetrics and Gynecology, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, Heilongjiang, China.
Background:
Ovarian cancer (OC) is a major cause of death among women due to the lack of early screening methods and its complex pathological progression. Increasing evidence has indicated that microRNAs regulate gene expression in tumours by interacting with mRNAs. Although the research regarding OC and microRNAs is extensive, the vital role of MIR502 in OC remains unclear.
Methods:
We integrated two microRNA expression arrays from GEO to identify differentially expressed genes. The Kaplan-Meier method was used to screen for miRNAs that had an influence on survival outcome. Upstream regulators of MIR502 were predicted by JASPAR and verified by ChIP-seq data. The LinkedOmics database was used to study genes that were correlated with MIR502. Gene Set Enrichment Analysis (GSEA) was conducted for functional annotation with GO and KEGG pathway enrichment analyses by using the open access WebGestalt tool. We constructed a PPI network by using STRING to further explore the core proteins.
Results:
We found that the expression level of MIR502 was significantly downregulated in OC, which was related to poor overall survival. NRF1, as an upstream regulator of MIR502, was predicted by JASPAR and verified by ChIP-seq data. In addition, anti-apoptosis and pro-proliferation genes in the Hippo signalling pathway, including CCND1, MYC, FGF1 and GLI2, were negatively regulated by MIR502, as shown in the GO and KEGG pathway enrichment results. The PPI network further demonstrated that CCND1 and MYCN were at core positions in the development of ovarian cancer.
Conclusions:
MIR502, which is regulated by NRF1, acts as a tumour suppressor gene to accelerate apoptosis and suppress proliferation by targeting the Hippo signalling pathway in ovarian cancer.
Insights
MicroRNA 502 (MIR502) acts as a tumor suppressor in ovarian cancer (OC) by inhibiting proliferation and promoting apoptosis via the Hippo signaling pathway. Its downregulation correlates with poor survival, and it is regulated by NRF1.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Ovarian cancer (OC) poses a significant mortality risk due to limited early detection and complex progression.
- MicroRNAs (miRNAs) are increasingly recognized for their role in regulating gene expression within tumors.
- The specific function of MIR502 in OC pathogenesis remains largely undefined.
Purpose of the Study:
- To investigate the role and regulatory mechanisms of MIR502 in ovarian cancer.
- To identify upstream regulators and downstream targets of MIR502.
- To elucidate the functional impact of MIR502 on OC development and survival.
Main Methods:
- Integrated miRNA expression arrays (GEO) to identify differentially expressed genes.
- Kaplan-Meier analysis for survival association.
- Bioinformatic prediction (JASPAR) and experimental validation (ChIP-seq) for upstream regulators.
- LinkedOmics database for gene correlation analysis.
- Gene Set Enrichment Analysis (GSEA) with GO and KEGG pathways (WebGestalt).
- Protein-protein interaction (PPI) network construction (STRING).
Main Results:
- MIR502 expression was significantly downregulated in OC, correlating with poorer overall survival.
- NRF1 was identified as a verified upstream regulator of MIR502.
- MIR502 negatively regulates pro-proliferation and anti-apoptosis genes (CCND1, MYC, FGF1, GLI2) within the Hippo signaling pathway.
- PPI network analysis highlighted CCND1 and MYCN as key players in OC development.
Conclusions:
- MIR502 functions as a tumor suppressor gene in ovarian cancer.
- NRF1 regulates MIR502, which in turn targets the Hippo signaling pathway.
- MIR502 promotes apoptosis and suppresses proliferation, offering potential therapeutic insights for OC.
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