beta-Adrenoreceptor antagonists reduce cancer cell proliferation, invasion, and migration

Area of Science:

• Pharmacology
• Cancer Biology
• Cellular Biology

Background:

• Non-selective beta-adrenergic receptor (AR) antagonists (propranolol, atenolol) and selective antagonists (ICI118,551 for β2-AR) are commonly used drugs.
• The role of ARs in non-stimulated cancer cell proliferation, migration, and invasion remains incompletely understood.

Purpose of the Study:

• To investigate the efficacy of propranolol, atenolol, and ICI118,551 on the proliferation, migration, and invasion of non-stimulated breast (MCF7), colon (HT-29), and hepatocellular (HepG2) cancer cells.
• To determine the impact of β-AR antagonism on key cancer cell behaviors.

Main Methods:

• Real-time PCR was used for β-AR expression profiling in cancer cell lines.
• Cell proliferation was assessed using the MTT assay.
• Cell invasion and migration were evaluated through Boyden chamber and scratch assays, respectively.

Main Results:

• All tested cancer cell lines (MCF7, HT-29, HepG2) expressed β-ARs.
• ICI118,551 exhibited the highest cytotoxicity, while atenolol was the least effective β-AR antagonist.
• ICI118,551 and propranolol significantly inhibited cancer cell invasion, with propranolol showing higher efficacy in HepG2 cells.
• All β-AR antagonists reduced cell migration to varying extents, influenced by concentration and incubation time.

Conclusions:

• The β2-AR antagonist ICI118,551 demonstrated the most significant cytotoxic effect on non-stimulated cancer cells.
• Propranolol and ICI118,551 were more potent in inhibiting invasion and migration compared to atenolol, suggesting a greater role for β2-ARs in these processes.
• The effectiveness of selective β-AR antagonists varied based on cell type, concentration, and incubation duration.