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Updated: Jun 6, 2025

3-D Cell Culture System for Studying Invasion and Evaluating Therapeutics in Bladder Cancer
Published on: September 13, 2018
Nucleolar protein 3 promotes proliferation of bladder cancer cells through the PI3K-Akt pathway
Linfeng Wu1, Kunyao Zhu1, Yan Sun1
1Department of Urology, The First Affiliated Hospital of Chongqing Medical University, 1 Youyi Road, Yuzhong District, Chongqing, 400016, P.R. China.
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.
Insights
Nucleolar protein 3 (NOL3) promotes bladder cancer (BLCA) cell proliferation. Inhibiting NOL3 halts cell cycle progression by suppressing the PI3K/Akt pathway, suggesting NOL3 as a therapeutic target for BLCA.
Area of Science:
- Oncology
- Molecular Biology
Background:
- Nucleolar protein 3 (NOL3) is upregulated in various cancers and known to play an anti-apoptotic role.
- Emerging research highlights NOL3's involvement in cancer metastasis and chemoresistance.
Purpose of the Study:
- To investigate the role of NOL3 in bladder cancer (BLCA) proliferation.
- To elucidate the underlying molecular mechanisms by which NOL3 influences BLCA cell growth.
Main Methods:
- Knockdown of NOL3 expression in two distinct BLCA cell lines.
- Cell cycle analysis to assess proliferation.
- Investigation of the PI3K/Akt signaling pathway.
- Pharmacological inhibition of PI3K using LY294002.
Main Results:
- NOL3 reduction significantly inhibited BLCA cell proliferation and induced stable cell cycle arrest.
- The PI3K/Akt pathway was found to be significantly inhibited upon NOL3 decrease.
- LY294002 treatment rescued NOL3 overexpression-induced PI3K/Akt activation and proliferation.
Conclusions:
- NOL3 is upregulated in BLCA and promotes cancer cell proliferation.
- NOL3 exerts its proliferative effects through the PI3K/Akt signaling pathway.
- NOL3 represents a potential therapeutic target for bladder cancer treatment.
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