hMSH6 deficiency and inactivation of the αE-catenin invasion-suppressor gene in HCT-8 colon cancer cells

Stefan J. Vermeulen, Philip R. Debruyne, Giancarlo Marra, Frank P. Speleman, Petra Boukamp, Josef Jiricny, Andrew P. Cuthbert, Robert F. Newbold, Friedel H. Nollet, Frans M. Van Roy, Marc M. Mareel*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Transition from an epithelioid (E) to a round (R) morphotype, in the human colon cancer cell line HCT-8, is associated with loss or truncation of αE-catenin and acquisition of invasiveness in organ culture. In E clones, like in parental HCT-8 cells, one allele of the αE-catenin gene (CTNNAI) is mutated. HCT-8 cells have also a 'Microsatelite Instability-High' (MSI-H) phenotype presumably due to a mutated hMSH6 gene. Fusion of E type cells doubles the wild type CTNNAI alleles and prevents the loss of αE-catenin. Introduction of an extra chromosome 2, carrying a wild type hMSH6 gene, restores post-replicative mismatch repair and also prevents the frequent inactivation of the remaining wild type CTNNAI allele.

Original languageEnglish
Pages (from-to)663-668
Number of pages6
JournalClinical and Experimental Metastasis
Volume17
Issue number8
DOIs
Publication statusPublished - 1999
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Keywords

  • αE-catenin
  • Cancer
  • Colorectal
  • hMSH6
  • Invasion

Fingerprint

Dive into the research topics of 'hMSH6 deficiency and inactivation of the αE-catenin invasion-suppressor gene in HCT-8 colon cancer cells'. Together they form a unique fingerprint.

Cite this