Beta-adrenergic blocker inhibits oral carcinogenesis and reduces tumor invasion

Heitor Pinhata Cecilio1, Vitor Bonetti Valente1, Karla Marcila Pereira1

  • 1Psychoneuroimmunology 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.

Abstract

Insights

Beta-blocker propranolol reduced oral cancer occurrence and thickness in a rat model. This suggests beta-adrenergic signaling plays a role in oral carcinogenesis and may be a target for cancer prevention.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Beta-adrenergic signaling is implicated in cancer progression.
  • Beta blockers are considered for adjuvant cancer therapy.
  • The role of beta-adrenergic blockers in tumorigenesis requires further investigation.

Purpose of the Study:

  • To investigate the effect of the beta-adrenergic blocker propranolol on oral tumor development.
  • To explore the impact of propranolol on oral squamous cell carcinoma (OSCC) onset and characteristics in a preclinical model.

Main Methods:

  • Male Wistar rats received daily propranolol or PBS injections.
  • Oral carcinogenesis was induced using 4-nitroquinoline-1-oxide (4NQO).
  • Tumor occurrence, volume, thickness, and cytokine levels (IL-6, TNF-α, IL-10) were assessed after 16 weeks.

Main Results:

  • Propranolol treatment decreased OSCC occurrence by 31% and significantly reduced tumor thickness.
  • Tumor volume was lower in propranolol-treated rats, though not statistically significant.
  • Propranolol reduced pro-inflammatory cytokines IL-6 and TNF-α in the tumor microenvironment.

Conclusions:

  • Beta-adrenergic signaling is involved in chemically induced oral carcinogenesis.
  • Propranolol demonstrates potential in reducing oral cancer development and associated inflammation.

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