TNFRSF11B promotes the progression of bladder cancer through PI3K/AKT signaling pathway
TNFRSF11B contributes to tumorigenesis in many malignancies. Nevertheless, its function and underlying tumorigenic mechanism in bladder cancer (BC) has been rare.The clinical significance and relevant signaling pathway of TNFRSF11B in BC were assessed using bioinformatic analysis. The determination...
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| Language: | English |
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Elsevier
2024-12-01
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| Series: | Molecular and Cellular Probes |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0890850824000410 |
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| author | Hao Deng Jinzhuo Ning Yuan Ruan Weimin Yu Fan Cheng |
| author_facet | Hao Deng Jinzhuo Ning Yuan Ruan Weimin Yu Fan Cheng |
| author_sort | Hao Deng |
| collection | DOAJ |
| description | TNFRSF11B contributes to tumorigenesis in many malignancies. Nevertheless, its function and underlying tumorigenic mechanism in bladder cancer (BC) has been rare.The clinical significance and relevant signaling pathway of TNFRSF11B in BC were assessed using bioinformatic analysis. The determination of TNFRSF11B expression was conducted in bladder tissues and BC cells. BC cells were subjected to functional experiments to evaluate their ability to proliferate, migrate, and invade. Cell apoptosis experiments were conducted. The protein levels of markers associated with epithelial-mesenchymal transition (EMT) and molecules linked to the PI3K/AKT pathway were assessed. To evaluate the effect of the PI3K/AKT pathway on TNFRSF11B, LY294002, a PI3K/AKT pathway inhibitor, was utilized. TNFRSF11B exhibited significant upregulation in both BC tissues and various cell lines. Inhibited TNFRSF11B expression impeded the growth, movement, infiltration of BC cells. Conversely, the ultimate outcome varied when TNFRSF11B was overexpressed. In vivo assay further confirmed the above results. Furthermore, TNFRSF11B promoted malignant traits by controlling the PI3K/AKT pathway. In BC, TNFRSF11B exhibits elevated expression levels and has a substantial tumor-promoting role in BC via the PI3K/AKT pathway. Importantly, TNFRSF11B may represent a valuable prognostic tumor marker for BC treatment. |
| format | Article |
| id | doaj-art-ee84619171f6499595b665952fb02e7c |
| institution | Kabale University |
| issn | 0890-8508 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Molecular and Cellular Probes |
| spelling | doaj-art-ee84619171f6499595b665952fb02e7c2024-12-17T04:58:49ZengElsevierMolecular and Cellular Probes0890-85082024-12-0178101989TNFRSF11B promotes the progression of bladder cancer through PI3K/AKT signaling pathwayHao Deng0Jinzhuo Ning1Yuan Ruan2Weimin Yu3Fan Cheng4Department of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060, China; Department of Urology, The First Affiliated Hospital of Yangtze University, Jingzhou, 434000, ChinaDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060, ChinaDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060, ChinaDepartment of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060, China; Corresponding author.Department of Urology, Renmin Hospital of Wuhan University, Wuhan, 430060, China; Corresponding author.TNFRSF11B contributes to tumorigenesis in many malignancies. Nevertheless, its function and underlying tumorigenic mechanism in bladder cancer (BC) has been rare.The clinical significance and relevant signaling pathway of TNFRSF11B in BC were assessed using bioinformatic analysis. The determination of TNFRSF11B expression was conducted in bladder tissues and BC cells. BC cells were subjected to functional experiments to evaluate their ability to proliferate, migrate, and invade. Cell apoptosis experiments were conducted. The protein levels of markers associated with epithelial-mesenchymal transition (EMT) and molecules linked to the PI3K/AKT pathway were assessed. To evaluate the effect of the PI3K/AKT pathway on TNFRSF11B, LY294002, a PI3K/AKT pathway inhibitor, was utilized. TNFRSF11B exhibited significant upregulation in both BC tissues and various cell lines. Inhibited TNFRSF11B expression impeded the growth, movement, infiltration of BC cells. Conversely, the ultimate outcome varied when TNFRSF11B was overexpressed. In vivo assay further confirmed the above results. Furthermore, TNFRSF11B promoted malignant traits by controlling the PI3K/AKT pathway. In BC, TNFRSF11B exhibits elevated expression levels and has a substantial tumor-promoting role in BC via the PI3K/AKT pathway. Importantly, TNFRSF11B may represent a valuable prognostic tumor marker for BC treatment.http://www.sciencedirect.com/science/article/pii/S0890850824000410BCTNFRSF11BPI3K/AKT |
| spellingShingle | Hao Deng Jinzhuo Ning Yuan Ruan Weimin Yu Fan Cheng TNFRSF11B promotes the progression of bladder cancer through PI3K/AKT signaling pathway Molecular and Cellular Probes BC TNFRSF11B PI3K/AKT |
| title | TNFRSF11B promotes the progression of bladder cancer through PI3K/AKT signaling pathway |
| title_full | TNFRSF11B promotes the progression of bladder cancer through PI3K/AKT signaling pathway |
| title_fullStr | TNFRSF11B promotes the progression of bladder cancer through PI3K/AKT signaling pathway |
| title_full_unstemmed | TNFRSF11B promotes the progression of bladder cancer through PI3K/AKT signaling pathway |
| title_short | TNFRSF11B promotes the progression of bladder cancer through PI3K/AKT signaling pathway |
| title_sort | tnfrsf11b promotes the progression of bladder cancer through pi3k akt signaling pathway |
| topic | BC TNFRSF11B PI3K/AKT |
| url | http://www.sciencedirect.com/science/article/pii/S0890850824000410 |
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