ArticleWorld journal of surgical oncology2024
Nucleolar protein 3 promotes proliferation of bladder cancer cells through the PI3K-Akt pathway.
Article in World journal of surgical oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Article
- Scalable differentiation of human cardiac organoids from iPSCs generates cardiac tissues for cardiac cell therapy.Theranostics · 2026Article
- The Role of NOL3 in Colon Adenocarcinoma Metastasis and Its Association With DNA Methylation.Human mutation · 2025Article
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Authors and funding
10 authors.
Funding
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Abstract
Nucleolar protein 3 (NOL3), as a markedly increased protein across a range of tumors, has been well acknowledged that plays an anti-apoptotic role in malignancies, while some novel impacts of NOL3 on metastasis and chemoresistance are demonstrated recently. In this study, we uncover another role of NOL3 on promoting proliferation in bladder cancer (BLCA). The reduction of NOL3 significantly inhibited cell proliferation, and we detected the stable cell cycle arrest after knockdown of NOL3 in two-type BLCA cell lines. Mechanistically, we present the first evidence that the PI3K/Akt pathway was considerably inhibited with the decrease of NOL3 in BLCA cell lines. In addition, LY294002, a PI3K inhibitor, rescued NOL3 overexpression-mediated activation of the PI3K/Akt axis and the depression of proliferation in BLCA cell lines. In conclusion, our study suggests that NOL3 is upregulated in BLCA cells and promotes proliferation via the PI3K/Akt pathway, indicating that NOL3 may be a potential therapeutic target for BLCA.
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