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Role of PAX2 in breast cancer verified by bioinformatics analysis and in vitro validation

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:...

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Autores principales: Yang, Shan, Gao, Wei, Wang, Haoqi, Zhang, Xi, Mi, Yunzhe, Ding, Yawen, Geng, Cuizhi, Zhang, Jie, Cheng, Meng, Li, Sainan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9929765/
https://www.ncbi.nlm.nih.gov/pubmed/36819548
http://dx.doi.org/10.21037/atm-22-6360
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author Yang, Shan
Gao, Wei
Wang, Haoqi
Zhang, Xi
Mi, Yunzhe
Ding, Yawen
Geng, Cuizhi
Zhang, Jie
Cheng, Meng
Li, Sainan
author_facet Yang, Shan
Gao, Wei
Wang, Haoqi
Zhang, Xi
Mi, Yunzhe
Ding, Yawen
Geng, Cuizhi
Zhang, Jie
Cheng, Meng
Li, Sainan
author_sort Yang, Shan
collection PubMed
description 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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spelling pubmed-99297652023-02-16 Role of PAX2 in breast cancer verified by bioinformatics analysis and in vitro validation Yang, Shan Gao, Wei Wang, Haoqi Zhang, Xi Mi, Yunzhe Ding, Yawen Geng, Cuizhi Zhang, Jie Cheng, Meng Li, Sainan Ann Transl Med Original Article 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. AME Publishing Company 2023-01-31 2023-01-31 /pmc/articles/PMC9929765/ /pubmed/36819548 http://dx.doi.org/10.21037/atm-22-6360 Text en 2023 Annals of Translational Medicine. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) .
spellingShingle Original Article
Yang, Shan
Gao, Wei
Wang, Haoqi
Zhang, Xi
Mi, Yunzhe
Ding, Yawen
Geng, Cuizhi
Zhang, Jie
Cheng, Meng
Li, Sainan
Role of PAX2 in breast cancer verified by bioinformatics analysis and in vitro validation
title Role of PAX2 in breast cancer verified by bioinformatics analysis and in vitro validation
title_full Role of PAX2 in breast cancer verified by bioinformatics analysis and in vitro validation
title_fullStr Role of PAX2 in breast cancer verified by bioinformatics analysis and in vitro validation
title_full_unstemmed Role of PAX2 in breast cancer verified by bioinformatics analysis and in vitro validation
title_short Role of PAX2 in breast cancer verified by bioinformatics analysis and in vitro validation
title_sort role of pax2 in breast cancer verified by bioinformatics analysis and in vitro validation
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9929765/
https://www.ncbi.nlm.nih.gov/pubmed/36819548
http://dx.doi.org/10.21037/atm-22-6360
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