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SETting Up for Epigenetic Regulation of Advanced Prostate Cancer

Phillip Thienger1, Mark A Rubin2

  • 1Department for BioMedical Research, University of Bern, Switzerland.

Cancer Cell
|September 15, 2020
PubMed

Insights

Therapy-resistant prostate cancer (PCa) can become more metastatic due to androgen receptor (AR) signaling inhibitors. A new study shows SETD2 regulates EZH2 and AMPK pathways, controlling PCa metastasis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Therapy-resistant prostate cancer (PCa) poses a significant clinical challenge.
  • Inhibitors of androgen receptor (AR) signaling can paradoxically promote cancer metastasis through epigenetic alterations.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying the enhanced metastatic potential of therapy-resistant prostate cancer.
  • To identify key regulators involved in epigenetic rewiring and metastasis.

Main Methods:

  • The study by Yuan et al. focuses on the role of the enzyme SETD2.
  • Investigated the integration of EZH2 and AMPK signaling pathways.

Main Results:

  • SETD2 plays a crucial role in regulating the metastatic potential of prostate cancer.
  • The integration of EZH2 and AMPK signaling by SETD2 is essential for controlling PCa metastasis.

Conclusions:

  • SETD2 acts as a critical checkpoint against prostate cancer metastasis.
  • Understanding SETD2's function offers potential therapeutic targets for advanced prostate cancer.

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