Transcriptional signature of Ecteinascidin 743 (Yondelis, Trabectedin) in human sarcoma cells explanted from chemo-naive patients

Mol Cancer Ther. 2005 May;4(5):814-23. doi: 10.1158/1535-7163.MCT-04-0316.

Abstract

Ecteinascidin 743 (ET-743; Yondelis, Trabectedin) is a marine anticancer agent that induces long-lasting objective remissions and tumor control in a subset of patients with pretreated/resistant soft-tissue sarcoma. Drug-induced tumor control is achievable in 22% of such patients, but there is no clear indication of the molecular features correlated with clinical sensitivity/resistance to ET-743. Nine low-passage, soft-tissue sarcoma cell lines, explanted from chemo-naive patients with different patterns of sensitivity, have been profiled with a cDNA microarray containing 6,700 cancer-related genes. The molecular signature of these cell lines was analyzed at baseline and at four different times after ET-743 exposure. The association of levels of TP53 mutation and TP73 expression with ET-743 sensitivity and cell cycle kinetics after treatment was also analyzed. Gene expression profile analysis revealed up-regulation of 86 genes and down-regulation of 244 genes in response to ET-743. The ET-743 gene expression signature identified a group of genes related with cell cycle control, stress, and DNA-damage response (JUNB, ATF3, CS-1, SAT, GADD45B, and ID2) that were up-regulated in all the cell lines studied. The transcriptional signature 72 hours after ET-743 administration, associated with ET-743 sensitivity, showed a more efficient induction of genes involved in DNA-damage response and apoptosis, such as RAD17, BRCA1, PAR4, CDKN1A, and P53DINP1, in the sensitive cell line group. The transcriptional signature described here may lead to the identification of ET-743 downstream mediators and transcription regulators and the proposal of strategies by which ET-743-sensitive tumors may be identified.

MeSH terms

  • Antineoplastic Agents, Alkylating / pharmacology*
  • Cell Cycle
  • Dioxoles / pharmacology*
  • Drug Resistance, Neoplasm*
  • Gene Expression Profiling*
  • Humans
  • Isoquinolines / pharmacology*
  • Kinetics
  • Mutation / genetics
  • Oligonucleotide Array Sequence Analysis
  • Sarcoma / genetics
  • Sarcoma / metabolism*
  • Tetrahydroisoquinolines
  • Trabectedin
  • Transcription, Genetic*
  • Tumor Cells, Cultured
  • Tumor Suppressor Protein p53 / genetics

Substances

  • Antineoplastic Agents, Alkylating
  • Dioxoles
  • Isoquinolines
  • Tetrahydroisoquinolines
  • Tumor Suppressor Protein p53
  • Trabectedin