Beta-adrenergic blocker inhibits oral carcinogenesis and reduces tumor invasion
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SHORT COMMUNICATION
Beta‑adrenergic blocker inhibits oral carcinogenesis and reduces tumor invasion Heitor Pinhata Cecilio1 · Vitor Bonetti Valente1 · Karla Marcila Pereira1 · Giseli Mitsuy Kayahara1,2 · Cristiane Furuse2 · Éder Ricardo Biasoli1,2 · Glauco Issamu Miyahara1,2 · Sandra Helena Penha Oliveira3 · Daniel Galera Bernabé1,2 Received: 1 July 2020 / Accepted: 16 September 2020 © Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Purpose Beta-adrenergic signaling can influence cancer progression and the use of beta blockers as adjuvant drugs in oncologic patients has been suggested. However, the involvement of beta-adrenergic blockers in tumorigenesis is poorly understood. This study investigated the action of beta-adrenergic blocker propranolol on tumor onset using a preclinical model of chemically induced oral cancer. Methods Thirty-two male Wistar rats were subjected to daily subcutaneous injection of beta-blocker propranolol (10 mg/ kg; SubQ), while another 32 rats received only a PBS injection (sham group). One week after starting propranolol treatment, all rats were submitted to chemical induction of oral carcinogenesis with 4-nitroquinoline-1-oxide (4NQO). After 16 weeks, they were assessed for occurrence of oral squamous cell carcinoma (OSCC), in addition to measurement of tumor volume and thickness, and tissue levels of cytokines IL-6, TNF-alpha and IL-10 in the tumor microenvironment. Results Propranolol treatment reduced the occurrence of OSCC by 31%, 95% CI ( − 127, 216). Beta-adrenergic blocker significantly decreased thickness of OSCC when compared with PBS. Rats treated with propranolol exhibited a lower tumor volume when compared with control rats, but this result did not reach statistical significance. Tumors from propranolol-treated rats exhibited reduced concentrations of pro-inflammatory cytokines IL-6 and TNF-α. There was no difference in the IL-10 levels between tumors from propranolol- and sham-treated rats. Conclusion Beta-adrenergic signaling may be one of the mechanisms associated with chemically induced oral carcinogenesis. Keywords Oral cancer · Carcinogenesis · Cancer progression · Propranolol · Beta-adrenergic antagonists
Introduction Clinical studies have shown that the chronic use of the non-selective beta blockers can affect cancer development [1–5]. Long-term beta-blocker therapy may reduce the * Daniel Galera Bernabé [email protected] 1
Psychoneuroimmunology Laboratory, Psychosomatic Research Center, Oral Oncology Center, São Paulo State University (Unesp), School of Dentistry, 1193 José Bonifácio St, Araçatuba, São Paulo 15050‑015, Brazil
2
Department of Diagnosis and Surgery, São Paulo State University (Unesp), School of Dentistry, 1193 José Bonifácio St, Araçatuba, São Paulo 15050‑015, Brazil
3
Immunopharmacology Laboratory, Department of Basic Sciences, São Paulo State University (Unesp), School of Dentistry, 1193 José Bonifácio St, Araçatuba, São Paulo 15050‑015, Brazil
incidence of prostate cancer [1] and improve the progn
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