PRR11 Promotes Bladder Cancer Growth and Metastasis by Facilitating G1/S Progression and Epithelial‐Mesenchymal Transition

ABSTRACT Background Although Proline‐rich Protein 11 (PRR11) abnormalities are closely associated with carcinogenesis, the precise mechanism of bladder cancer remains unclear. Here, we sought to elucidate the molecular mechanisms of PRR11 in bladder cancer. Methods We performed differential expressi...

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Main Authors: Lu Wang, Zengshun Kou, Jiaxi Zhu, Xiu Zhu, Lei Gao, Hai Zhu
Format: Article
Language:English
Published: Wiley 2025-03-01
Series:Cancer Medicine
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Online Access:https://doi.org/10.1002/cam4.70749
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author Lu Wang
Zengshun Kou
Jiaxi Zhu
Xiu Zhu
Lei Gao
Hai Zhu
author_facet Lu Wang
Zengshun Kou
Jiaxi Zhu
Xiu Zhu
Lei Gao
Hai Zhu
author_sort Lu Wang
collection DOAJ
description ABSTRACT Background Although Proline‐rich Protein 11 (PRR11) abnormalities are closely associated with carcinogenesis, the precise mechanism of bladder cancer remains unclear. Here, we sought to elucidate the molecular mechanisms of PRR11 in bladder cancer. Methods We performed differential expression analysis of PRR11 from the TCGA and GEO databases, followed by validation with clinical samples. Survival analysis was employed to assess the correlation between PRR11 and patient prognosis. The effects of PRR11 on bladder cancer cells were examined through both in vitro and in vivo experiments. Additionally, Gene Set Enrichment Analysis (GSEA) was used to predict the downstream pathways associated with PRR11, which were further validated through subsequent experiments. Results PRR11 is upregulated in bladder cancer and could lead to poor prognosis. In vitro, PRR11 promoted tumor cell proliferation; in vivo, it promoted subcutaneous tumor growth. PRR11 knockdown inhibited its oncogenic function. On the molecular level, PRR11 promotes tumor metastasis by inducing Epithelial‐mesenchymal Transition (EMT). GSEA suggests that PRR11 is strongly linked to the cell cycle, and silencing of PRR11 can achieve anti‐tumor effects by inhibiting CCNE and blocking the G1/S phase transition. Conclusions Our study demonstrates that silencing PRR11 can arrest the malignant progression of bladder cancer by inhibiting EMT and blocking the G1/S transition. Targeting PRR11 may provide new insights for targeting cell cycle therapy.
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spelling doaj-art-52a435daddc84f9cbba3ac7c3efd00f62025-08-20T02:59:07ZengWileyCancer Medicine2045-76342025-03-01145n/an/a10.1002/cam4.70749PRR11 Promotes Bladder Cancer Growth and Metastasis by Facilitating G1/S Progression and Epithelial‐Mesenchymal TransitionLu Wang0Zengshun Kou1Jiaxi Zhu2Xiu Zhu3Lei Gao4Hai Zhu5Department of Urology, Qingdao Municipal Hospital University of Health and Rehabilitation Sciences Qingdao ChinaDepartment of Urology, Qingdao Municipal Hospital University of Health and Rehabilitation Sciences Qingdao ChinaLife Sciences, Faculty of Arts & Science University of Toronto‐St. George Campus Toronto CanadaFaculty of Information Science and Engineering Ocean University of China Qingdao ChinaDepartment of Urology, Qingdao Municipal Hospital University of Health and Rehabilitation Sciences Qingdao ChinaDepartment of Urology, Qingdao Municipal Hospital University of Health and Rehabilitation Sciences Qingdao ChinaABSTRACT Background Although Proline‐rich Protein 11 (PRR11) abnormalities are closely associated with carcinogenesis, the precise mechanism of bladder cancer remains unclear. Here, we sought to elucidate the molecular mechanisms of PRR11 in bladder cancer. Methods We performed differential expression analysis of PRR11 from the TCGA and GEO databases, followed by validation with clinical samples. Survival analysis was employed to assess the correlation between PRR11 and patient prognosis. The effects of PRR11 on bladder cancer cells were examined through both in vitro and in vivo experiments. Additionally, Gene Set Enrichment Analysis (GSEA) was used to predict the downstream pathways associated with PRR11, which were further validated through subsequent experiments. Results PRR11 is upregulated in bladder cancer and could lead to poor prognosis. In vitro, PRR11 promoted tumor cell proliferation; in vivo, it promoted subcutaneous tumor growth. PRR11 knockdown inhibited its oncogenic function. On the molecular level, PRR11 promotes tumor metastasis by inducing Epithelial‐mesenchymal Transition (EMT). GSEA suggests that PRR11 is strongly linked to the cell cycle, and silencing of PRR11 can achieve anti‐tumor effects by inhibiting CCNE and blocking the G1/S phase transition. Conclusions Our study demonstrates that silencing PRR11 can arrest the malignant progression of bladder cancer by inhibiting EMT and blocking the G1/S transition. Targeting PRR11 may provide new insights for targeting cell cycle therapy.https://doi.org/10.1002/cam4.70749biomarkersbladder cancercell cyclePRR11tumor treatment
spellingShingle Lu Wang
Zengshun Kou
Jiaxi Zhu
Xiu Zhu
Lei Gao
Hai Zhu
PRR11 Promotes Bladder Cancer Growth and Metastasis by Facilitating G1/S Progression and Epithelial‐Mesenchymal Transition
Cancer Medicine
biomarkers
bladder cancer
cell cycle
PRR11
tumor treatment
title PRR11 Promotes Bladder Cancer Growth and Metastasis by Facilitating G1/S Progression and Epithelial‐Mesenchymal Transition
title_full PRR11 Promotes Bladder Cancer Growth and Metastasis by Facilitating G1/S Progression and Epithelial‐Mesenchymal Transition
title_fullStr PRR11 Promotes Bladder Cancer Growth and Metastasis by Facilitating G1/S Progression and Epithelial‐Mesenchymal Transition
title_full_unstemmed PRR11 Promotes Bladder Cancer Growth and Metastasis by Facilitating G1/S Progression and Epithelial‐Mesenchymal Transition
title_short PRR11 Promotes Bladder Cancer Growth and Metastasis by Facilitating G1/S Progression and Epithelial‐Mesenchymal Transition
title_sort prr11 promotes bladder cancer growth and metastasis by facilitating g1 s progression and epithelial mesenchymal transition
topic biomarkers
bladder cancer
cell cycle
PRR11
tumor treatment
url https://doi.org/10.1002/cam4.70749
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