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 language | English |
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Pages (from-to) | 663-668 |
Number of pages | 6 |
Journal | Clinical and Experimental Metastasis |
Volume | 17 |
Issue number | 8 |
DOIs | |
Publication status | Published - 1999 |
Externally published | Yes |
ASJC Scopus subject areas
- Oncology
- Cancer Research
Keywords
- αE-catenin
- Cancer
- Colorectal
- hMSH6
- Invasion