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A2B adenosine receptor blockade inhibits growth of prostate cancer cells

Qiang Wei1, Stefano Costanzi, Ramachandran Balasubramanian

  • 1Molecular Recognition Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0810, USA.

Purinergic Signalling
|January 15, 2013
PubMed

Insights

Blockade of the A2B adenosine receptor (AR) inhibits prostate cancer cell growth. This suggests that A2B AR antagonists could be a novel therapeutic strategy for prostate cancer treatment.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Adenosine receptors (ARs) play diverse roles in cellular functions.
  • The A2B adenosine receptor subtype is highly expressed in common prostate cancer cell lines.

Purpose of the Study:

  • To investigate the role of the A2B adenosine receptor (AR) in prostate cancer cell death and proliferation.
  • To evaluate the therapeutic potential of A2B AR antagonists in prostate cancer.

Main Methods:

  • Gene expression analysis (RT-PCR, Western blot) of AR subtypes in prostate cancer cell lines (PC-3, DU145, LNCaP).
  • Functional studies using A2B AR agonists (NECA, BAY60-6583) and antagonists (PSB603) in PC-3 cells.
  • Assessment of apoptosis markers (LDH release, caspase-3 activity), cyclic AMP accumulation, and cell proliferation (siRNA).

Main Results:

  • A2B AR exhibited the highest gene expression among AR subtypes in PC-3, DU145, and LNCaP cells.
  • A2B AR activation by agonists increased cyclic AMP levels and protected against apoptosis.
  • A2B AR blockade with PSB603 inhibited cell growth across all tested prostate cancer cell lines.

Conclusions:

  • The A2B adenosine receptor is implicated in the regulation of prostate cancer cell growth.
  • Selective A2B AR antagonists demonstrate efficacy in inhibiting prostate cancer cell proliferation.
  • A2B AR antagonists represent a promising therapeutic avenue for prostate cancer treatment.

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