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Author Spotlight: Exploring the Role of FAM83A in Cervical Cancer
Published on: February 9, 2024
E2F8 knockdown suppresses cell proliferation and induces cell cycle arrest via Wnt/β-Catenin pathway in ovarian
Meiyin Zhang1, Ye Xu1, Yongjian Zhang1
1Department of Gynecology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China.
Abstract:
Ovarian cancer is one of the leading causes of death in female reproductive system cancers. However, the pathogenesis of ovarian cancer remains elusive. Our aim is to investigate the potential targets for ovarian cancer. Two microarray datasets were obtained from the Gene Expression Omnibus public database. Using R package limma, the differentially expressed genes (DEGs) were identified from the datasets. There were 95 overlapping DEGs in two microarray datasets. GO, KEGG pathway analysis, and protein-protein interaction (PPI) network analysis were carried out based on the DEGs. Wnt signaling pathway and cell cycle were enriched in the KEGG pathway analysis. Moreover, the top 10 hub genes with the most nodes were determined by PPI network analysis. E2F8, one of hub genes was positively linked to a bad outcome in ovarian cancer patients. Furthermore, E2F8 knockdown suppressed cell proliferation and induced cell cycle arrest in ovarian cancer. In addition, we found that silencing E2F8 inhibited the Wnt/β-catenin signaling pathway. In ovarian cancer cells with E2F8 knockdown, overexpressing β-catenin restored both the suppressed capacity of cell proliferation and cell cycle progression. Therefore, our results revealed that E2F8 had an involvement in the development of ovarian cancer which might act as a therapeutic target.
Insights
This study identifies E2F8 as a key gene in ovarian cancer development. Silencing E2F8 inhibits tumor growth and progression by affecting the Wnt/β-catenin pathway, suggesting E2F8 as a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Ovarian cancer is a leading cause of cancer death in women, with its underlying mechanisms not fully understood.
- Identifying novel therapeutic targets is crucial for improving patient outcomes.
Purpose of the Study:
- To investigate potential molecular targets for ovarian cancer therapy.
- To elucidate the role of differentially expressed genes in ovarian cancer pathogenesis.
Main Methods:
- Analysis of two Gene Expression Omnibus microarray datasets to identify differentially expressed genes (DEGs).
- Utilized R package limma for DEG identification, followed by Gene Ontology (GO), KEGG pathway, and protein-protein interaction (PPI) network analyses.
- Investigated the functional role of identified hub genes, specifically E2F8, through knockdown experiments and pathway analysis.
Main Results:
- Identified 95 overlapping DEGs across two datasets, with Wnt signaling pathway and cell cycle enrichment.
- Determined E2F8 as a top hub gene, significantly associated with poor prognosis in ovarian cancer patients.
- E2F8 knockdown suppressed ovarian cancer cell proliferation, induced cell cycle arrest, and inhibited the Wnt/β-catenin signaling pathway.
Conclusions:
- E2F8 plays a significant role in ovarian cancer development and progression.
- The Wnt/β-catenin signaling pathway is implicated in E2F8's function.
- E2F8 represents a promising therapeutic target for ovarian cancer treatment.
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