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Induction of invasion in vivo of α‐catenin‐positive HCT‐8 human colon‐cancer cells
Author(s) -
Van Hoorde Leen,
Pocard Marc,
Maryns Isabelle,
Poupon MarieFrance,
Mareel Marc
Publication year - 2000
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/1097-0215(20001201)88:5<751::aid-ijc11>3.0.co;2-b
Subject(s) - in vivo , in vitro , catenin , colorectal cancer , cancer research , cell culture , biology , cancer , cecum , cancer cell , pathology , wnt signaling pathway , microbiology and biotechnology , medicine , biochemistry , signal transduction , ecology , genetics
Variants from the HCT‐8 colon‐cancer cell line were implanted s.c. and orthotopically into nude mice. Well‐differentiated HCT‐8/E11 and HCT‐8/E41 cells have a functional E‐cadherin–catenin complex and are non‐invasive into pre‐cultured chick heart fragments in vitro, whereas poorly differentiated HCT‐8/E11R1 cells are deficient in α‐catenin protein and invasive in heart fragments. We investigated whether these differences were maintained in vivo. In contrast with in vitro observations, in vivo the 3 HCT‐8 variants behaved very similarly and all formed undifferentiated tumors. The in vivo invasive behavior of HCT‐8 cells was site‐dependently modulated: HCT‐8 cells invaded when injected into the cecum but not when injected s.c. Metastases to the liver or lungs were not observed. The composition and expression of the E‐cadherin–catenin complex in nude mouse HCT‐8 tumors was the same as in HCT‐8 cells in culture on solid substrate. We conclude that the in vivo invasive behavior of HCT‐8 cells is not determined by whether α‐catenin is expressed or not but by as yet unidentified host factors. Int. J. Cancer 88:751–758, 2000. © 2000 Wiley‐Liss, Inc.