Target disruption of the mutant β-catenin gene in colon cancer cell line HCT116: Preservation of its malignant phenotype

Shigeki Sekine, Tatsuhiro Shibata, Michiie Sakamoto, Setsuo Hirohashi

研究成果: Article査読

35 被引用数 (Scopus)

抄録

Most colorectal carcinomas harbor genetic alterations that result in stabilization of β-catenin. A colorectal carcinoma cell line, HCT116, which has both mutated and wild-type β-catenin genes, was engineered by homologous recombination to investigate the significance of β-catenin gene mutation. As expected, the mutant allele-targeted clones showed decreased β-catenin expression and downregulation of T-cell factor (TCF)/lymphoid enhancer factor (LEF)-dependent transcription. Morphologically, targeted clones were only minimally altered under usual culture conditions, but under low serum conditions, mutant allele-targeted clones still grew in plane, in contrast to parental cell line and wild allele-targeted clones, which formed spheroids. The mutant allele-targeted clones showed no significant changes in growth rate and anchorage-independent growth hi vitro, and displayed rather increased growth in vivo. Although β-catenin stabilization affects some biological characteristics including adhesive properties, it may not have growth-promoting effects at least in some colorectal carcinomas.

本文言語English
ページ(範囲)5906-5911
ページ数6
ジャーナルOncogene
21
38
DOI
出版ステータスPublished - 2002 8 29

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research

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