The antitumor effect of PLK1 and HSF1 double knockdown on human oral carcinoma cells

Int J Oncol. 2010 Apr;36(4):867-72. doi: 10.3892/ijo_00000564.

Abstract

High levels of mitotic progression-associated PLK1 and stress-associated HSF1 have been observed in various human cancers. In the present study, we investigated the effects of PLK1 and HSF1 knockdown on the proliferation of oral cancer cells using small interfering RNA. In human oral squamous cell carcinoma (SCC) tissues, the levels of PLK1 and HSF1 were higher compared to normal tissues. The expression levels of PLK1 and HSF1 were also elevated in the human oral SCC cell lines FaDu and HEp-2. Disruption of PLK1 induced cell cycle arrest at G2/M phase as well as apoptosis in oral cancer cells. Interestingly, knockdown of both PLK1 and HSF1 expression decreased cell proliferation while increasing apoptotic cell death in synergistic fashion. These results establish the potential value of PLK1 and HSF1 as targets for oral cancer therapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / genetics
  • Carcinoma, Squamous Cell / enzymology
  • Carcinoma, Squamous Cell / genetics
  • Carcinoma, Squamous Cell / pathology
  • Carcinoma, Squamous Cell / therapy*
  • Cell Cycle / genetics
  • Cell Cycle Proteins / genetics*
  • Cell Cycle Proteins / metabolism
  • Cell Line, Tumor
  • Cell Proliferation*
  • Cell Survival
  • DNA-Binding Proteins / genetics*
  • DNA-Binding Proteins / metabolism
  • Down-Regulation
  • Gene Knockdown Techniques*
  • Genetic Therapy / methods*
  • Heat Shock Transcription Factors
  • Heat-Shock Proteins / metabolism
  • Hot Temperature
  • Humans
  • Hypopharyngeal Neoplasms / enzymology
  • Hypopharyngeal Neoplasms / genetics
  • Hypopharyngeal Neoplasms / pathology
  • Hypopharyngeal Neoplasms / therapy*
  • Laryngeal Neoplasms / enzymology
  • Laryngeal Neoplasms / genetics
  • Laryngeal Neoplasms / pathology
  • Laryngeal Neoplasms / therapy*
  • Polo-Like Kinase 1
  • Protein Serine-Threonine Kinases / genetics*
  • Protein Serine-Threonine Kinases / metabolism
  • Proto-Oncogene Proteins / genetics*
  • Proto-Oncogene Proteins / metabolism
  • RNA Interference*
  • Transcription Factors / genetics*
  • Transcription Factors / metabolism

Substances

  • Cell Cycle Proteins
  • DNA-Binding Proteins
  • HSF1 protein, human
  • Heat Shock Transcription Factors
  • Heat-Shock Proteins
  • Proto-Oncogene Proteins
  • Transcription Factors
  • Protein Serine-Threonine Kinases