CENPN contributes to pancreatic carcinoma progression through the MDM2-mediated p53 signaling pathway
Introduction We undertook an in-depth investigation of the data pertaining to pancreatic adenocarcinoma (PAAD) to identify potential targets for the development of precision therapies. Material and methods The construction of a protein-protein interaction (PPI) network was based on overlapping diff...
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| Format: | Article |
| Language: | English |
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Termedia Publishing House
2024-04-01
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| Series: | Archives of Medical Science |
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| Online Access: | https://www.archivesofmedicalscience.com/CENPN-contributes-to-pancreatic-carcinoma-progression-through-the-MDM2-mediated-p53,171956,0,2.html |
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| _version_ | 1832584852873936896 |
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| author | Ming Xu Jie Tang Qiong Sun Jing Meng Guoyu Chen Yunli Chang Yao Yao Jieru Ji Hao Luo Lingling Chen Minxue Lu Weiwei Shi |
| author_facet | Ming Xu Jie Tang Qiong Sun Jing Meng Guoyu Chen Yunli Chang Yao Yao Jieru Ji Hao Luo Lingling Chen Minxue Lu Weiwei Shi |
| author_sort | Ming Xu |
| collection | DOAJ |
| description | Introduction
We undertook an in-depth investigation of the data pertaining to pancreatic adenocarcinoma (PAAD) to identify potential targets for the development of precision therapies.
Material and methods
The construction of a protein-protein interaction (PPI) network was based on overlapping differentially expressed genes (DEGs) identified in the GSE16515, GSE32676, and GSE125158 datasets. A subsequent bioinformatic analysis was performed on the interconnected genes within the PPI network, leading to the identification of the central gene, CENPN. In vitro experimentation such as CCK8 and Transwell experiments was employed to elucidate the impact of CENPN expression patterns on PAAD cell proliferation, migration, and invasion. Furthermore, the investigation revealed through comprehensive enrichment analysis that the pivotal signaling pathway associated with CENPN is the p53 signaling pathway.
Results
Following a comprehensive bioinformatic analysis of 161 concordant differentially expressed genes (DEGs) across three microarray datasets, CENPN emerged as the central gene under investigation. Overexpression of CENPN in pancreatic adenocarcinoma (PAAD) was associated with unfavorable patient outcomes and heightened sensitivity to four PAAD therapies: gemcitabine, docetaxel, paclitaxel, and sunitinib. Reduced CENPN expression impeded PAAD cell proliferation, migration, and invasion; however, these effects were counteracted upon upregulation of CENPN expression. Additionally, CENPN interacted with MDM2, promoting PAAD progression by targeting the p53 signaling pathway.
Conclusions
The findings of our study substantiate that CENPN is associated with the pathogenesis of PAAD. Consequently, CENPN appears to be a promising candidate for targeted precision therapy in clinical applications. |
| format | Article |
| id | doaj-art-3cee0bbaa42e4dc698f66853cf6fea74 |
| institution | Kabale University |
| issn | 1734-1922 1896-9151 |
| language | English |
| publishDate | 2024-04-01 |
| publisher | Termedia Publishing House |
| record_format | Article |
| series | Archives of Medical Science |
| spelling | doaj-art-3cee0bbaa42e4dc698f66853cf6fea742025-01-27T10:44:31ZengTermedia Publishing HouseArchives of Medical Science1734-19221896-91512024-04-012051655167110.5114/aoms/171956171956CENPN contributes to pancreatic carcinoma progression through the MDM2-mediated p53 signaling pathwayMing Xu0Jie Tang1Qiong Sun2Jing Meng3Guoyu Chen4Yunli Chang5Yao Yao6Jieru Ji7Hao Luo8Lingling Chen9Minxue Lu10Weiwei Shi11Department of Gastroenterology, Shanghai Pudong New Area People’s Hospital, Shanghai, ChinaDepartment of Gastroenterology, Shanghai Pudong New Area People’s Hospital, Shanghai, ChinaDepartment of Oncology, The First Medical Center, Chinese PLA General Hospital, Beijing, ChinaDepartment of Oncology, The First Medical Center, Chinese PLA General Hospital, Beijing, ChinaDepartment of Gastroenterology, Shanghai Pudong New Area People’s Hospital, Shanghai, ChinaDepartment of Gastroenterology, Shanghai Pudong New Area People’s Hospital, Shanghai, ChinaDepartment of Gastroenterology, Shanghai Pudong New Area People’s Hospital, Shanghai, ChinaDepartment of Gastroenterology, Shanghai Pudong New Area People’s Hospital, Shanghai, ChinaDepartment of Gastroenterology, Shanghai Pudong New Area People’s Hospital, Shanghai, ChinaDepartment of Gastroenterology, Shanghai Pudong New Area People’s Hospital, Shanghai, ChinaDepartment of Gastroenterology, Huzhou College Affiliated Nantaihu Hospital, Huzhou, Zhejiang, ChinaDepartment of Oncology, The First Medical Center, Chinese PLA General Hospital, Beijing, ChinaIntroduction We undertook an in-depth investigation of the data pertaining to pancreatic adenocarcinoma (PAAD) to identify potential targets for the development of precision therapies. Material and methods The construction of a protein-protein interaction (PPI) network was based on overlapping differentially expressed genes (DEGs) identified in the GSE16515, GSE32676, and GSE125158 datasets. A subsequent bioinformatic analysis was performed on the interconnected genes within the PPI network, leading to the identification of the central gene, CENPN. In vitro experimentation such as CCK8 and Transwell experiments was employed to elucidate the impact of CENPN expression patterns on PAAD cell proliferation, migration, and invasion. Furthermore, the investigation revealed through comprehensive enrichment analysis that the pivotal signaling pathway associated with CENPN is the p53 signaling pathway. Results Following a comprehensive bioinformatic analysis of 161 concordant differentially expressed genes (DEGs) across three microarray datasets, CENPN emerged as the central gene under investigation. Overexpression of CENPN in pancreatic adenocarcinoma (PAAD) was associated with unfavorable patient outcomes and heightened sensitivity to four PAAD therapies: gemcitabine, docetaxel, paclitaxel, and sunitinib. Reduced CENPN expression impeded PAAD cell proliferation, migration, and invasion; however, these effects were counteracted upon upregulation of CENPN expression. Additionally, CENPN interacted with MDM2, promoting PAAD progression by targeting the p53 signaling pathway. Conclusions The findings of our study substantiate that CENPN is associated with the pathogenesis of PAAD. Consequently, CENPN appears to be a promising candidate for targeted precision therapy in clinical applications.https://www.archivesofmedicalscience.com/CENPN-contributes-to-pancreatic-carcinoma-progression-through-the-MDM2-mediated-p53,171956,0,2.htmlpancreatic adenocarcinomacenpnmdm2p53 signaling pathway |
| spellingShingle | Ming Xu Jie Tang Qiong Sun Jing Meng Guoyu Chen Yunli Chang Yao Yao Jieru Ji Hao Luo Lingling Chen Minxue Lu Weiwei Shi CENPN contributes to pancreatic carcinoma progression through the MDM2-mediated p53 signaling pathway Archives of Medical Science pancreatic adenocarcinoma cenpn mdm2 p53 signaling pathway |
| title | CENPN contributes to pancreatic carcinoma progression through the MDM2-mediated p53 signaling pathway |
| title_full | CENPN contributes to pancreatic carcinoma progression through the MDM2-mediated p53 signaling pathway |
| title_fullStr | CENPN contributes to pancreatic carcinoma progression through the MDM2-mediated p53 signaling pathway |
| title_full_unstemmed | CENPN contributes to pancreatic carcinoma progression through the MDM2-mediated p53 signaling pathway |
| title_short | CENPN contributes to pancreatic carcinoma progression through the MDM2-mediated p53 signaling pathway |
| title_sort | cenpn contributes to pancreatic carcinoma progression through the mdm2 mediated p53 signaling pathway |
| topic | pancreatic adenocarcinoma cenpn mdm2 p53 signaling pathway |
| url | https://www.archivesofmedicalscience.com/CENPN-contributes-to-pancreatic-carcinoma-progression-through-the-MDM2-mediated-p53,171956,0,2.html |
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