Detection of differentially expressed HES-6 gene in metastatic colon carcinoma by combination of suppression subtractive hybridization and cDNA library array

Cancer Lett. 2003 Aug 20;198(2):229-39. doi: 10.1016/s0304-3835(03)00313-6.

Abstract

The molecular mechanisms involved in the progression of colon carcinomas from a primary to a metastatic tumor have been only partially elucidated and poorly understood. This study combines suppression subtractive hybridization and cDNA array hybridization to identify genes with expression differences between a primary human colon tumor cell line (HT29) and three isogenic lung tumor metastases. The positive clones isolated in this screen were further validated and quantitated with real-time reverse transcription polymerase chain reactions. HES-6 was identified as up-regulated in each of the individual tumor metastases, as well as in a panel of primary human tumors derived from the lung, breast and kidney. These findings demonstrate that it is possible to utilize longitudinal samples from an in vivo model of colon carcinoma to identify genes up-regulated in metastases and that HES-6 may be an important marker of a range of primary cancers as well as metastatic colon carcinoma.

MeSH terms

  • Animals
  • Base Sequence
  • Basic Helix-Loop-Helix Transcription Factors
  • Breast Neoplasms / genetics
  • Chromosome Aberrations*
  • Colonic Neoplasms / genetics*
  • Colonic Neoplasms / pathology
  • DNA Primers
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Gene Library
  • Humans
  • Kidney Neoplasms / genetics
  • Lung Neoplasms / genetics
  • Mice
  • Mice, Nude
  • Neoplasm Metastasis
  • Nucleic Acid Hybridization / methods
  • Oligonucleotide Array Sequence Analysis
  • Ovarian Neoplasms / genetics
  • Repressor Proteins*
  • Transcription Factors / genetics*
  • Transplantation, Heterologous
  • Tumor Cells, Cultured

Substances

  • Basic Helix-Loop-Helix Transcription Factors
  • DNA Primers
  • HES6 protein, human
  • Hes6 protein, mouse
  • Repressor Proteins
  • Transcription Factors