Identification of the expression profile of apoptotic esophageal cancer cells by adenoviral-fragile histidine triad treatment

Koshi Mimori, Hideshi Ishii, Hiroshi Inoue, Graham F. Barnard, Masaki Mori

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1 Citation (Scopus)

Abstract

Background: The fragile histidine triad (FHIT) functions as a tumor suppressor, and giving adenoviral-FHIT (Ad-FHIT) is thus expected to be clinically beneficial. Much attention has recently been focused on which genes are commonly regulated by Ad-FHIT, and which genes are dominant in Ad-FHIT-induced apoptotic cells. Methods: Ad-FHIT apoptosis-induced cells (H1299 and TE4) and non-apoptosis-induced cells (TE2) were used in the current experiments. The total RNA extracted from Ad-FHIT or control was labeled with Cy3-dCTP or Cy5-dCTP and hybridized with 19 192 genes on a chip. A microarray analysis for each gene was carried out with high reproducibility provided by seven independent experiments and duplicated oligos on a chip. Results: We listed the upregulated genes based on the TE4:TE2 expression ratio, such as c-Src, Jak-1, and sialyltransferase, which are expected to be target pathways as well as the downregulated genes, including CASP8 and CASP10, after Ad-FHIT treatment in esophageal cancer. Conclusions: The current microarray analysis indicated that the apoptosis of esophageal cancer observed after giving Ad-FHIT was possibly induced by activation of the c-Src gene and inactivation of the CASP8 gene.

Original languageEnglish
JournalJournal of Gastroenterology and Hepatology (Australia)
Volume23
Issue numberSUPPL. 2
DOIs
Publication statusPublished - Jan 1 2008

All Science Journal Classification (ASJC) codes

  • Hepatology
  • Gastroenterology

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