Wenrui Tang, Lin Wang, Xudong Yan, Jisheng Zhang, Longgang Yu, Han Chen, Chunge Zheng, Zihui Dong, Qianyou Zheng, Lin Han, Yan Jiang
{"title":"Secreted phosphoprotein 1 is associated with epithelial cell proliferation and PI3K/AKT signalling in sinonasal inverted papilloma.","authors":"Wenrui Tang, Lin Wang, Xudong Yan, Jisheng Zhang, Longgang Yu, Han Chen, Chunge Zheng, Zihui Dong, Qianyou Zheng, Lin Han, Yan Jiang","doi":"10.1177/20503121261445213","DOIUrl":null,"url":null,"abstract":"<p><strong>Objectives: </strong>Sinonasal inverted papilloma is a locally aggressive epithelial lesion with a relatively high recurrence rate, yet the molecular basis of its proliferative behaviour remains incompletely understood. This study investigated the clinical relevance of secreted phosphoprotein 1 in sinonasal inverted papilloma and its association with epithelial cell proliferation and related signalling pathways.</p><p><strong>Methods: </strong>Differentially expressed genes were identified from the GSE193016 dataset, followed by gene set enrichment analysis. The expression of secreted phosphoprotein 1 and the cell cycle-related molecules cell division cycle 25C and cyclin A2 in clinical specimens was assessed using quantitative PCR, Western blotting, and immunohistochemistry. Associations between secreted phosphoprotein 1 expression and postoperative recurrence were assessed based on follow-up data. In vitro experiments using human nasal epithelial cells were conducted to examine the effects of altered secreted phosphoprotein 1 expression on cell proliferation-associated phenotypes, and pathway inhibition assays were performed to investigate the involvement of the PI3K/AKT signalling pathway.</p><p><strong>Results: </strong>Secreted phosphoprotein 1 expression was significantly upregulated in sinonasal inverted papilloma tissues, with higher levels observed in advanced-stage cases (T3-T4), and was associated with postoperative recurrence. The expression of the cell cycle-related molecules cell division cycle 25C and cyclin A2, positively correlated with secreted phosphoprotein 1 expression and increased with disease progression. In vitro epithelial cell models demonstrated that modulation of secreted phosphoprotein 1 expression was accompanied by corresponding changes in cellular proliferative capacity and cell cycle-related protein expression. Pathway inhibition assays further suggested that PI3K/AKT signalling may be involved in secreted phosphoprotein 1-associated alterations in cell cycle regulation.</p><p><strong>Conclusion: </strong>These findings indicate that secreted phosphoprotein 1 is highly expressed in sinonasal inverted papilloma and may be associated with epithelial cell proliferation and PI3K/AKT signalling. In addition, secreted phosphoprotein 1 expression correlates with disease recurrence, highlighting its potential research value as a biological marker, while the underlying mechanisms warrant further investigation.</p>","PeriodicalId":21398,"journal":{"name":"SAGE Open Medicine","volume":"14 ","pages":"20503121261445213"},"PeriodicalIF":2.2000,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13145016/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"SAGE Open Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1177/20503121261445213","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0
Abstract
Objectives: Sinonasal inverted papilloma is a locally aggressive epithelial lesion with a relatively high recurrence rate, yet the molecular basis of its proliferative behaviour remains incompletely understood. This study investigated the clinical relevance of secreted phosphoprotein 1 in sinonasal inverted papilloma and its association with epithelial cell proliferation and related signalling pathways.
Methods: Differentially expressed genes were identified from the GSE193016 dataset, followed by gene set enrichment analysis. The expression of secreted phosphoprotein 1 and the cell cycle-related molecules cell division cycle 25C and cyclin A2 in clinical specimens was assessed using quantitative PCR, Western blotting, and immunohistochemistry. Associations between secreted phosphoprotein 1 expression and postoperative recurrence were assessed based on follow-up data. In vitro experiments using human nasal epithelial cells were conducted to examine the effects of altered secreted phosphoprotein 1 expression on cell proliferation-associated phenotypes, and pathway inhibition assays were performed to investigate the involvement of the PI3K/AKT signalling pathway.
Results: Secreted phosphoprotein 1 expression was significantly upregulated in sinonasal inverted papilloma tissues, with higher levels observed in advanced-stage cases (T3-T4), and was associated with postoperative recurrence. The expression of the cell cycle-related molecules cell division cycle 25C and cyclin A2, positively correlated with secreted phosphoprotein 1 expression and increased with disease progression. In vitro epithelial cell models demonstrated that modulation of secreted phosphoprotein 1 expression was accompanied by corresponding changes in cellular proliferative capacity and cell cycle-related protein expression. Pathway inhibition assays further suggested that PI3K/AKT signalling may be involved in secreted phosphoprotein 1-associated alterations in cell cycle regulation.
Conclusion: These findings indicate that secreted phosphoprotein 1 is highly expressed in sinonasal inverted papilloma and may be associated with epithelial cell proliferation and PI3K/AKT signalling. In addition, secreted phosphoprotein 1 expression correlates with disease recurrence, highlighting its potential research value as a biological marker, while the underlying mechanisms warrant further investigation.