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Pan-caner analysis identifies PSMA7 as a targets for amplification at 20q13.33 in tumorigenesis
Guangying Sheng1,2, Fuyu Li1,2,3, Wen Jin1
1State Key Laboratory of Medical Genomics, Ruijin Hospital Shanghai Institute of Hematology, National Research Center for Translational Medicine at Shanghai, Shanghai Jiao Tong University School of Medicine, 197 Ruijin Er Rd, Shanghai, 200025, China.
Abstract:
The chromosome 20 long arm (20q) is one of the genomic hotspots where copy number alterations frequently occur in multiple types of tumors. However, it remains elusive which genes are implicated in 20q-related tumorigenesis. Here, by querying TCGA and GEO databases, we observed frequent copy number amplification at 20q and the chromosome subband 20q13.33 was amplificated in multiple cancers. Among those genes at 20q13.33, PSMA7 was found with the strongest correlation with cancers. Further analysis revealed that PSMA7 amplification was the most frequent genetic alteration event conferring adverse prognosis in various cancers. Consistent with the strong positive correlation between PSMA7 amplification and gene expression, elevated PSMA7 expression was observed in 20 of 33 types of cancers with a close link to adverse outcomes in certain tumors. In addition, PSMA7 was essential for the growth of almost 1095 cancer lines. Mechanistically, aberrant PSMA7 most probably influenced the proteasome and protease-related pathways to promote tumorigenesis and might be antagonized by several compounds, e.g., Docetaxel in relevant cancers. The current in-depth pan-cancer analysis refines our understanding of the crucial oncogenic role of copy number amplifications at PSMA7 loci at the novel chromosome amplicon 20q13.33 across different tumors.
Insights
Copy number amplifications in chromosome 20q, specifically at 20q13.33, frequently occur in cancers. PSMA7 gene amplification is strongly linked to cancer development and poor prognosis, highlighting its oncogenic role.
Area of Science:
- Genomics
- Cancer Biology
- Oncology
Background:
- Chromosome 20 long arm (20q) is a known genomic hotspot for copy number alterations in various tumors.
- The specific genes driving 20q-related tumorigenesis remain largely unidentified.
- Understanding these alterations is crucial for targeted cancer therapies.
Purpose of the Study:
- To identify genes within the frequently amplified 20q13.33 chromosomal subband that are implicated in tumorigenesis.
- To investigate the oncogenic role of PSMA7 amplification and its correlation with cancer progression and patient outcomes.
- To explore the mechanistic pathways influenced by PSMA7 and potential therapeutic interventions.
Main Methods:
- Utilized TCGA and GEO databases for comprehensive genomic analysis.
- Performed copy number alteration and gene expression correlation analysis.
- Assessed the essentiality of PSMA7 in cancer cell line growth and analyzed its association with proteasome/protease pathways.
Main Results:
- Frequent copy number amplifications were observed at 20q, particularly the 20q13.33 subband across multiple cancer types.
- PSMA7 amplification showed the strongest correlation with cancer and was the most frequent genetic alteration linked to adverse prognosis.
- Elevated PSMA7 expression, correlating with amplification, was found in 20 of 33 cancer types, associated with poorer outcomes.
- PSMA7 was essential for the growth of 1095 cancer cell lines, likely through proteasome and protease pathways.
- Docetaxel was identified as a potential antagonist to PSMA7 in relevant cancers.
Conclusions:
- PSMA7 amplification at the 20q13.33 locus is a significant oncogenic driver across diverse cancers.
- Elevated PSMA7 expression and its role in proteasome/protease pathways contribute to tumorigenesis and adverse outcomes.
- PSMA7 represents a potential therapeutic target, with compounds like Docetaxel showing promise for antagonism.
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