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The expression and clinical significance of ARHGAP25 in osteosarcoma based on bioinformatics analysis
Xiaoqian Liu1, Siyuan Zhang1, Dong Wang1
1First Affiliated Hospital Trauma Center, Hainan Medical University, Haikou, 570100, China.
Abstract:
ARHGAP25, a member of the ARHGAP family, encodes a negative regulator of Rho-GTPase that is important for actin remodeling, cell polarity, and cell migration. ARHGAP25 is down-regulated in a variety of solid tumors and promotes cancer cell growth, migration, and invasion. However, nothing is understood about ARHGAP25's biological function in osteosarcoma. This work used qPCR and WB to confirm the expression of ARHGAP25 in osteosarcoma following the initial analysis of its expression in pan-cancer. For GO and KEGG analysis, we have chosen 300 genes from the TARGET osteosarcoma data that had the strongest positive correlation with ARHGAP25, and we created nomogram and calibration charts. We simultaneously overexpressed ARHGAP25 in osteosarcoma cells to examine its impact on apoptosis and proliferation. By using MSP, we determined their methylation status in osteosarcoma cells and normal bone cells. We observed that ARHGAP25 was significantly downregulated in a range of malignancies, including osteosarcoma, and was associated with poor patient outcomes. The decrease of ARHGAP25 expression in osteosarcoma is related to DNA methylation. Overexpression of ARHGAP25 induced apoptosis and inhibited the proliferation of osteosarcoma cells in vitro. In addition, ARHGAP25 is also associated with immune-related pathways in osteosarcoma. These findings suggest that ARHGAP25 is a valuable prognostic biomarker in osteosarcoma patients.
Insights
ARHGAP25, a regulator of cell functions, is downregulated in osteosarcoma and linked to poor outcomes. Its reduced expression, due to DNA methylation, inhibits cancer cell proliferation and promotes apoptosis, suggesting it as a prognostic biomarker.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- ARHGAP25 regulates Rho-GTPase, impacting actin remodeling, cell polarity, and migration.
- ARHGAP25 is downregulated in various solid tumors, promoting cancer progression.
- The role of ARHGAP25 in osteosarcoma remains largely uncharacterized.
Purpose of the Study:
- To investigate the biological function and prognostic significance of ARHGAP25 in osteosarcoma.
- To explore the correlation between ARHGAP25 expression, DNA methylation, and patient outcomes.
- To assess the impact of ARHGAP25 overexpression on osteosarcoma cell behavior.
Main Methods:
- Quantitative PCR (qPCR) and Western Blot (WB) for gene expression analysis.
- Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis.
- Methylation-Specific PCR (MSP) to determine DNA methylation status.
- In vitro overexpression studies in osteosarcoma cells.
Main Results:
- ARHGAP25 was significantly downregulated in osteosarcoma and associated with poor patient prognosis.
- Decreased ARHGAP25 expression in osteosarcoma is linked to DNA methylation.
- Overexpression of ARHGAP25 induced apoptosis and inhibited proliferation of osteosarcoma cells in vitro.
- ARHGAP25 expression correlated with immune-related pathways in osteosarcoma.
Conclusions:
- ARHGAP25 functions as a tumor suppressor in osteosarcoma.
- ARHGAP25 is a potential prognostic biomarker for osteosarcoma patients.
- DNA methylation is a key mechanism for ARHGAP25 downregulation in osteosarcoma.
