Rare activation of the TCF/beta-catenin pathway in ovarian cancer

Gynecol Oncol. 2000 Apr;77(1):97-104. doi: 10.1006/gyno.1999.5718.

Abstract

Objective: The activation of the T cell factor/beta-catenin pathway is a crucial event in colon cancer initiation. A recent report describing the presence of beta-catenin mutations in endometrioid ovarian cancer suggested that the TCF/beta-catenin pathway may be generally activated in ovarian cancer. We therefore undertook to determine the frequency of activation of this pathway in ovarian cancer cell lines using a functional screen.

Methods: We functionally screened a series of ovarian cancer cell lines for the presence of constitutive TCF/beta-catenin-mediated transcriptional activity using a reporter assay. Lines possessing such activity were subjected to mutational and gel-shift analysis, as well as sensitivity to the introduction of dominant-negative TCF or APC alleles. A cDNA harboring a beta-catenin point mutation found in an ovarian cancer line was incorporated into an expression plasmid for functional analysis.

Results: Constitutive TCF/beta-catenin transcriptional activity was detected in 21% (4 of 19) of ovarian lines studied, while 32% (6 of 19) exhibited greater than twofold repression. One of the constitutively active lines, UCI107, harbored an activating beta-catenin point mutation, which was shown to be capable of inducing TCF/beta-catenin transcriptional activity in transiently transfected 293 cells. A second active line, SW626, was shown to harbor an inactivating APC mutation and may in fact be of colonic origin. The third and fourth lines harbored neither an APC nor a beta-catenin mutation. Gel-shift analysis, together with the absence of sensitivity to dominant-negative TCF, indicated that the reporter activity exhibited by the latter two cell lines may not be due to a TCF/beta-catenin transcriptional complex.

Conclusions: These results indicate that genuine constitutive activation of the TCF/beta-catenin pathway is infrequent in ovarian cancer, but that constitutive transcriptional repression from TCF sites is more common in this tumor type.

MeSH terms

  • Cytoskeletal Proteins / genetics*
  • DNA Mutational Analysis*
  • DNA Primers / chemistry
  • DNA, Neoplasm / analysis*
  • DNA-Binding Proteins / genetics*
  • Female
  • Humans
  • Lymphoid Enhancer-Binding Factor 1
  • Ovarian Neoplasms / genetics*
  • Ovarian Neoplasms / metabolism
  • Ovarian Neoplasms / pathology
  • Point Mutation
  • Trans-Activators*
  • Transcription Factors / genetics*
  • Transcription, Genetic
  • Transcriptional Activation*
  • Transfection
  • Tumor Cells, Cultured
  • beta Catenin

Substances

  • CTNNB1 protein, human
  • Cytoskeletal Proteins
  • DNA Primers
  • DNA, Neoplasm
  • DNA-Binding Proteins
  • Lymphoid Enhancer-Binding Factor 1
  • Trans-Activators
  • Transcription Factors
  • beta Catenin