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FBXO45 Knockdown Restrains the Progression of Bladder Cancer via the ERK/Cyclin D1/CDK4 Pathway

Weiyang Zhang1, Qingyuan Liu1, Jindong Zhang1

  • 1Department of Urology, The First Affiliated Hospital of Chongqing Medical University, 400016 Chongqing, China.

Archivos Espanoles De Urologia
|September 6, 2024
PubMed
Abstract

Insights

F-box protein 45 (FBXO45) promotes bladder cancer progression by enhancing cell proliferation and migration. Silencing FBXO45 inhibits tumor growth and induces apoptosis, offering a potential therapeutic target for bladder cancer.

Area of Science:

  • Oncology
  • Molecular Biology

Background:

  • F-box protein 45 (FBXO45) is linked to various diseases.
  • Its role in bladder cancer development is not well understood.

Purpose of the Study:

  • To investigate the role of FBXO45 in the malignant progression of bladder cancer cells.
  • To elucidate the underlying molecular mechanisms.

Main Methods:

  • FBXO45 was silenced in bladder cancer cell lines (RT4 and 5637) using small-interference fragments.
  • Cell proliferation, migration, invasion, apoptosis, and cell cycle were assessed.
  • Key protein levels in the ERK/Cyclin D1/CDK4 pathway were analyzed via Western blot.

Main Results:

  • FBXO45 knockdown significantly inhibited bladder cancer cell proliferation, migration, and invasion (p < 0.01).
  • Silencing FBXO45 reduced S-phase cells and increased apoptosis (p < 0.01).
  • FBXO45 knockdown decreased the expression of p-ERK1/2, CDK4, and Cyclin D1 (p < 0.01).

Conclusions:

  • FBXO45 acts as an oncoprotein in bladder cancer.
  • The ERK/Cyclin D1/CDK4 pathway is involved in FBXO45-mediated bladder cancer progression.
  • FBXO45 may serve as a potential therapeutic target for bladder cancer treatment.
Keywords:
ERK/Cyclin D1/CDK4FBXO45bladder cancercell cycleproliferation

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