Up-regulation of C-terminal tensin-like molecule promotes the tumorigenicity of colon cancer through β-catenin

Yi Chun Liao, Nien Tsu Chen, Yi Ping Shih, Ying Dong, Su Hao Lo

Research output: Contribution to journalArticle

37 Scopus citations

Abstract

C-terminal tensin-like (cten) is a focal adhesion molecule belonging to the tensin family. Previous studies have suggested that cten may function as a prostate-specific tumor suppressor. Here, we show that although cten is expressed at a very low level in normal colon, its expression is significantly up-regulated in colon cancer. Furthermore, a high population of cten is found in the nucleus, where it interacts with β-catenin, a critical player in the canonical Wnt pathway. This interaction may contribute to the role of cten in enhancing the colony formation, anchorage-independent growth, and invasiveness of colon cancer cells. Our studies have identified cten as a novel nuclear partner of β-catenin, showed an oncogenic activity of cten in colon cancers, and revealed cten as a potential biomarker and target for colon cancers.

Original languageEnglish (US)
Pages (from-to)4563-4566
Number of pages4
JournalCancer Research
Volume69
Issue number11
DOIs
StatePublished - Jun 1 2009

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Fingerprint Dive into the research topics of 'Up-regulation of C-terminal tensin-like molecule promotes the tumorigenicity of colon cancer through β-catenin'. Together they form a unique fingerprint.

  • Cite this