The bacterial protein azurin enhances sensitivity of oral squamous carcinoma cells to anticancer drugs

Yonsei Med J. 2011 Sep;52(5):773-8. doi: 10.3349/ymj.2011.52.5.773.

Abstract

Purpose: Surgical therapy is the primary treatment for oral cancer, but it can cause facial distortion. Therefore, if anticancer drugs are effective against oral cancer, they may be used preferentially. However, oral squamous carcinoma cells (OSCCs) are resistant to these drugs, so finding a way to enhance the sensitivity of these cells to anticancer drugs is important. The bacterial protein azurin is known to selectively enter cancer cells and induce apoptosis. In this study, we show the anticancer effect of azurin in OSCC.

Materials and methods: OSCC cell line (YD-9) was subjected to azurin treatment. Cell viability, morphology and protein expression levels were monitored after treatment of azurin. Cells were also subjected to combination treatment of azurin with either 5-fluorouracil or etopside.

Results: Azurin-treated cells showed decreased cell viability accompanied by apoptotic phenotypes including morphological change, DNA breakage, and increases in p53 and cyclin B1 protein levels. Combination treatment of azurin with other anti-tumor agents caused an increase in sensitivity to anticancer drugs in azurin-treated YD-9 cells.

Conclusion: Azurin has a strong synergistic anticancer effect on oral cancer cells when it is used along with anticancer drugs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / administration & dosage*
  • Apoptosis / drug effects
  • Azurin / administration & dosage*
  • Azurin / genetics
  • Carcinoma, Squamous Cell / drug therapy*
  • Carcinoma, Squamous Cell / metabolism
  • Carcinoma, Squamous Cell / pathology
  • Cell Line, Tumor
  • Cyclin B1 / metabolism
  • Drug Synergism
  • Etoposide / administration & dosage
  • Fluorouracil / administration & dosage
  • Humans
  • Mouth Neoplasms / drug therapy*
  • Mouth Neoplasms / metabolism
  • Mouth Neoplasms / pathology
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Antineoplastic Agents
  • CCNB1 protein, human
  • Cyclin B1
  • TP53 protein, human
  • Tumor Suppressor Protein p53
  • Azurin
  • Etoposide
  • Fluorouracil