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Multidrug resistance gene 1 expression in salivary gland adenocarcinomas and oral squamous-cell carcinomas

T Uematsu1, T Hasegawa, B Y Hiraoka

  • 1Department of Oral and Maxillofacial Surgery, Matsumoto Dental University School of Dentistry, Shiojiri, Nagano 399-0781, Japan.

Insights

Salivary gland adenocarcinoma (SGA) exhibits inherent multidrug resistance (MDR) due to P-glycoprotein (P-gp) induction and production. Oral squamous cell carcinoma (SCC) develops MDR primarily through P-gp induction, impacting head-and-neck cancer chemotherapy outcomes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Salivary gland adenocarcinoma (SGA) shows poor outcomes in head-and-neck cancer (HNC) chemotherapy.
  • P-glycoprotein (P-gp) mediated multidrug resistance (MDR) is a potential factor differentiating drug sensitivity between SGA and oral squamous cell carcinoma (SCC).

Purpose of the Study:

  • To investigate the association between P-gp expression and MDR in HNC.
  • To elucidate the distinct mechanisms of P-gp development in SGA versus SCC.

Main Methods:

  • Immunohistochemical analysis of P-gp expression in normal salivary glands, oral mucosa, and HNC tissues.
  • In vivo chemotherapeutic models using tumor-bearing nude mice.
  • RT-PCR to assess mdr1 mRNA expression levels in cell lines after vincristine (VCR) treatment.

Main Results:

  • P-gp was expressed in salivary gland ductal cells but not oral epithelium; intensive P-gp expression was observed in SGA compared to SCC.
  • In vivo models showed P-gp expression developed in both HSY (SGA) and Hepd (SCC) cell lines after VCR treatment.
  • RT-PCR revealed significantly higher mdr1 mRNA levels in VCR-treated HSY clones compared to Hepd clones, indicating differential P-gp induction and production.

Conclusions:

  • P-gp-related MDR in SGA is an inherent phenotype, driven by high P-gp induction and activated production during chemotherapy.
  • P-gp-related MDR in SCC is primarily an acquired phenotype, mainly resulting from P-gp induction.
  • Understanding these differential mechanisms is crucial for improving HNC treatment strategies.

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