TrkB-Targeted Therapy for Mucoepidermoid Carcinoma

Vivian P Wagner1,2, Manoela D Martins1,3, Esra Amoura2

  • 1Department of Oral Diagnosis, Piracicaba Dental School, University of Campinas, Piracicaba 13414-903, Brazil.

Biomedicines
|December 1, 2020
PubMed

Insights

TrkB inhibition impaired mucoepidermoid carcinoma (MEC) cell migration and survival. While ANA-12 reduced cancer stem cells (CSCs), Cisplatin was more effective, though combination therapy led to CSC recovery, a limiting factor.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The brain-derived neurotrophic factor (BDNF)/tyrosine receptor kinase B (TrkB) pathway is implicated in adenocarcinoma oncogenesis.
  • The role of the BDNF/TrkB pathway in mucoepidermoid carcinoma (MEC) remains underexplored.

Purpose of the Study:

  • To investigate the role of the BDNF/TrkB pathway in MEC.
  • To evaluate the efficacy of TrkB inhibition, alone and in combination with Cisplatin, on MEC cell behavior.

Main Methods:

  • Utilized three MEC cell lines (UM-HMC-2, H253, H292).
  • Treated cells with Cisplatin, the TrkB inhibitor ANA-12, or a combination.
  • Assessed ultrastructural changes via transmission electron microscopy.
  • Evaluated migration and invasion using scratch and Transwell assays.
  • Determined survival and cancer stem cell (CSC) percentage via clonogenic and spheroid-forming assays.

Main Results:

  • Cisplatin induced significant cytotoxicity and reduced CSCs.
  • ANA-12 demonstrated less pronounced cytotoxicity but reduced CSCs.
  • Both drugs individually and in combination delayed MEC cell migration, invasion, and survival.
  • Combination therapy showed less reduction in CSCs compared to Cisplatin alone, with subsequent recovery of spheroid-forming capacity.

Conclusions:

  • TrkB inhibition effectively impairs MEC cell migration, invasion, and survival in vitro.
  • The combined treatment's limited efficacy in reducing CSCs compared to Cisplatin alone is a significant limitation.
  • Further research is needed to optimize combination therapies for MEC treatment targeting the BDNF/TrkB pathway.

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