ArticleAnnals of translational medicine2023
Role of PAX2 in breast cancer verified by bioinformatics analysis and
Article in Annals of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- PAX2 induces endometrial cancer by inhibiting mitochondrial function via the CD133-AKT1 pathway.Molecular and cellular biochemistry · 2025Article
- Truncated O-glycosylation in metastatic triple-negative breast cancer reveals a gene expression signature associated with extracellular matrix and proteolysis.Scientific reports · 2024Article
- Liposomal Nano-Based Drug Delivery Systems for Breast Cancer Therapy: Recent Advances and Progresses.Anti-cancer agents in medicinal chemistry · 2024Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Breast cancer (BC) is the most frequently diagnosed cancer in women and the second most common cancer among newly diagnosed cancers worldwide. Studies have shown that paired box 2 (PAX2) participates in the tumorigenesis of some cancer cells, but its role in BC is still unclear. Methods: Transcriptome expression profiles and clinicopathological information of BC were downloaded from The Cancer Genome Atlas (TCGA) database to explore the expression level and prognostic value of PAX2. Gene set enrichment analysis (GSEA) and functional enrichment analysis were performed to investigate the functions and pathways of PAX2. Moreover, real-time reverse transcriptase-polymerase chain reaction (RT-qPCR) was used to determine the expression of PAX2 in BC tissues, and the predictive value of PAX2 in clinical samples was assessed. Cell Counting Kit-8 (CCK-8) assay was used to evaluate cell growth. The migration and invasive capacities of cells were assessed by wound healing assay and Transwell assay. Results: PAX2 was upregulated in the TCGA-BC datasets. GSEA suggested that PAX2 may be involved in the regulation of signaling pathways such as MAPK. Moreover, PAX2 was overexpressed in BC tissues, and PAX2 expression was associated with tumor size and lymph node metastasis. PAX2 deficiency could promote the growth, migration, and invasion of BC cells. Conclusions: Upregulation of PAX2 inhibited BC cell growth, migration, and invasion, making PAX2 a potential therapeutic target for BC.
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