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.

PubMed

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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