DOPAMINERGIC STIMULATION AND β-ADRENERGIC BLOCKADE ATTENUATE DMBA-INDUCED MAMMARY TUMOUR GROWTH

The global burden of breast cancer necessitates innovative adjunct therapies to address conventional treatment limitations. This study investigated the antitumour potential of repurposing propranolol (β-adrenergic blocker) and dopamine (dopaminergic agonist) in comparison with tamoxifen, utilizing a DMBA-induced mammary carcinoma rat model. In this preclinical in vivo study, sixty female albino rats were enrolled; fifty rats underwent mammary tumour induction and, upon developing palpable tumours, were allocated into five treatment groups (n=10 per group), while the remaining ten rats served as plain controls. Assessment parameters include tumour volume, proliferative (Ki-67) and apoptotic (Caspase-3) markers, serum VEGF, and hepatic oxidative stress (MDA and GSH). Findings revealed that dopamine and tamoxifen significantly suppressed tumour growth by week four, while propranolol exhibited a moderate effect. Tamoxifen and dopamine effectively suppressed cellular proliferation, as indicated by reduced Ki-67 expression. Furthermore, all interventions successfully triggered apoptosis, evidenced by significantly elevated Caspase-3 levels. Notably, dopamine exhibited the most potent anti-angiogenic profile, restoring serum VEGF to near-normal concentrations. While tamoxifen and propranolol effectively mitigated hepatic oxidative stress, dopamine displayed limited antioxidant efficacy. In conclusion, the present findings indicate that the pharmacological targeting of β-adrenergic and dopaminergic signalling cascades yields significant antitumour efficacy. These pathways represent highly promising candidates for adjunct breast cancer management, justifying more extensive clinical evaluations of these repurposed therapeutic agents.