Altered phenotype of HT29 colonic adenocarcinoma cells following expression of the DCC gene

Anna Velcich, Georgia Corner, Lisa Palumbo, Leonard Augenlicht

Research output: Contribution to journalArticle

34 Scopus citations

Abstract

On 18q, frequently deleted in late stage colorectal cancers, a gene, Deleted in Colon Cancer (DCC), has been identified and postulated to play a role as a tumor suppressor gene. DCC is retained in the majority of mucinous tumors, which produce high levels of mucins, and seems to be preferentially expressed in intestinal goblet cells. To investigate whether DCC is related to mucin expression and can modulate the transformed phenotype, we introduced a full-length DCC cDNA into HT29 cells, which can be induced in vitro to express MUC2, the gene that encodes the major colonic mucin. Expression of DCC did not modulate constitutive or induced expression of MUC2, nor did DCC induce a mature goblet cell phenotype. However, HT29 clones expressing high and low levels of DCC protein showed a significant decrease in cell proliferation and tumorigenicity. Furthermore, increased shedding and an elevated rate of spontaneous apoptosis were associated with higher levels of expression of DCC. In summary, while restoration of DCC expression in a human colon carcinoma cell line did not influence expression of differentiation markers, DCC expression did affect the growth and tumorigenic properties of the cells suggesting that DCC can modulate the malignant phenotype of colon cancer.

Original languageEnglish (US)
Pages (from-to)2599-2606
Number of pages8
JournalOncogene
Volume18
Issue number16
DOIs
StatePublished - Apr 22 1999

Keywords

  • Colon cancer
  • DCC
  • MUC2 expression

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

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