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An Orthotopic Murine Model of Human Prostate Cancer Metastasis
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An Orthotopic Murine Model of Human Prostate Cancer Metastasis

Published on: September 18, 2013

Apigenin inhibits prostate cancer progression in TRAMP mice via targeting PI3K/Akt/FoxO pathway

Sanjeev Shukla1, Natarajan Bhaskaran, Melissa A Babcook

  • 1Department of Urology, Case Western Reserve University and The Urology Institute, University Hospitals Case Medical Center, Cleveland, OH 44106, USA.

Carcinogenesis
|September 27, 2013
PubMed

Insights

Apigenin, a plant flavone, suppresses prostate cancer growth and metastasis in mice by targeting the PI3K/Akt/FoxO pathway. This natural compound reduces tumor volume and prevents distant organ spread by modulating key cell cycle regulators.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Forkhead box O (FoxO) transcription factors are crucial tumor suppressors in human cancers.
  • Prostate cancer often involves disrupted FoxO activity due to PTEN loss and PI3K/Akt activation.
  • Apigenin, a plant flavone, shows anticancer potential, but its mechanisms are not fully understood.

Purpose of the Study:

  • To investigate the efficacy of apigenin in suppressing prostate tumorigenesis.
  • To elucidate the role of the PI3K/Akt/FoxO signaling pathway in apigenin's anticancer effects.
  • To evaluate apigenin's impact on tumor growth, metastasis, and cell cycle regulation in prostate cancer models.

Main Methods:

  • Treatment of TRAMP mice and human prostate cancer cell lines (LNCaP, PC-3) with apigenin.
  • Assessment of tumor volume, metastasis, and organ weights in treated mice.
  • Analysis of PI3K/Akt/FoxO signaling pathway components, including phosphorylation and nuclear retention.
  • Evaluation of cell proliferation markers (Ki-67, cyclin D1) and FoxO-responsive proteins (BIM, p27/Kip1).
  • Cell cycle analysis to determine arrest points.

Main Results:

  • Apigenin significantly reduced prostate tumor volumes and abolished distant metastasis in TRAMP mice.
  • Apigenin treatment decreased PI3K/Akt pathway activation, evidenced by reduced Akt and FoxO3a phosphorylation.
  • Apigenin enhanced FoxO3a nuclear retention, increased expression of BIM and p27/Kip1, and induced G0/G1 cell cycle arrest in cancer cells.
  • In vitro studies confirmed apigenin's effects on human prostate cancer cells, mimicking PI3K/Akt inhibitor actions.

Conclusions:

  • Apigenin effectively suppresses prostate cancer progression and metastasis in vivo and in vitro.
  • The mechanism involves targeting the PI3K/Akt/FoxO signaling pathway, leading to reduced proliferation and cell cycle arrest.
  • Apigenin represents a potential therapeutic agent for prostate cancer, leveraging its ability to modulate key oncogenic signaling pathways.

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