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Published on: September 15, 2023
Human pan-cancer analysis of the predictive biomarker for the CDKN3
Yingjun Chen1, Dai Li2, Kaihui Sha3
1Department of Infectious Diseases, Binzhou Medical University Hospital, Binzhou, 256600, Shandong, China.
Background:
Cell cycle protein-dependent kinase inhibitor protein 3 (CDKN3), as a member of the protein kinase family, has been demonstrated to exhibit oncogenic properties in several tumors. However, there are no pan-carcinogenic analyses for CDKN3.
Methods:
Using bioinformatics tools such as The Cancer Genome Atlas (TCGA) and the UCSC Xena database, a comprehensive pan-cancer analysis of CDKN3 was conducted. The inverstigation encompassed the examination of CDKN3 function actoss 33 different kinds of tumors, as well as the exploration of gene expressions, survival prognosis status, clinical significance, DNA methylation, immune infiltration, and associated signal pathways.
Results:
CDKN3 was significantly upregulated in most of tumors and correlated with overall survival (OS) of patients. Methylation levels of CDKN3 differed significantly between tumors and normal tissues. In addition, infiltration of CD4 + T cells, cancer-associated fibroblasts, macrophages, and endothelial cells were associated with CDKN3 expression in various tumors. Mechanistically, CDKN3 was associated with P53, PI3K-AKT, cell cycle checkpoints, mitotic spindle checkpoint, and chromosome maintenance.
Conclusion:
Our pan-cancer analysis conducted in the study provides a comprehensive understanding of the involvement of CDKN3 gene in tumorigenesis. The findings suggest that targeting CDKN3 may potentially lead to novel therapeutic strategies for the treatment of tumors.
Insights
Cell cycle protein-dependent kinase inhibitor protein 3 (CDKN3) is upregulated in most cancers and linked to patient survival. Targeting CDKN3 may offer new cancer treatment strategies.
Area of Science:
- Oncology
- Molecular Biology
- Bioinformatics
Background:
- Cell cycle protein-dependent kinase inhibitor protein 3 (CDKN3) exhibits oncogenic properties in several tumors.
- No comprehensive pan-cancer analyses for CDKN3 have been previously conducted.
Purpose of the Study:
- To conduct a comprehensive pan-cancer analysis of CDKN3.
- To investigate CDKN3's role in tumorigenesis across 33 tumor types.
Main Methods:
- Utilized bioinformatics tools including The Cancer Genome Atlas (TCGA) and UCSC Xena database.
- Examined gene expression, survival prognosis, clinical significance, DNA methylation, and immune infiltration related to CDKN3.
- Investigated signaling pathways associated with CDKN3.
Main Results:
- CDKN3 was significantly upregulated in most tumors and correlated with overall survival (OS).
- Significant differences in CDKN3 methylation levels were observed between tumor and normal tissues.
- CDKN3 expression was associated with the infiltration of CD4+ T cells, cancer-associated fibroblasts, macrophages, and endothelial cells.
- CDKN3 mechanistically linked to P53, PI3K-AKT, cell cycle checkpoints, mitotic spindle checkpoint, and chromosome maintenance.
Conclusions:
- The pan-cancer analysis provides a comprehensive understanding of CDKN3's involvement in tumorigenesis.
- Targeting CDKN3 presents potential for novel therapeutic strategies in cancer treatment.
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