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Oncogenic beta-catenin signaling networks in colorectal cancer.
- Source :
-
Cell cycle (Georgetown, Tex.) [Cell Cycle] 2005 Nov; Vol. 4 (11), pp. 1522-39. Date of Electronic Publication: 2005 Dec 01. - Publication Year :
- 2005
-
Abstract
- Beta-catenin has two distinct functions, namely, maintaining cell-to-cell adhesion and mediating the Wnt/beta-catenin signal transduction pathway, which plays pivotal roles in embryogenesis and in malignant transformation of cells. The oncogenic properties of Wnt/beta-catenin signaling stem from alteration in phosphorylation-dependent protein degradation and subcellular localization of beta-catenin from cell membrane to the nucleus, where it binds to T-cell factor (Tcf) to form a bipartite transcription factor. The beta-catenin/Tcf complex facilitates transcription of target genes that encode effectors for activation of cell proliferation and invasion and inhibition of apoptosis, leading to colorectal cancer development. In addition, in the tumor invasion front, stabilized and activated beta-catenin interacts with other molecular pathways to facilitate tumor progression. This review highlights the beta-catenin-dependent oncogenic signaling network involved in the multi-step process of colorectal tumorigenesis. Wnt signaling evidently regulates stem cells, leading them to differentiate or self-renew. We address roles of oncogenic beta-catenin signaling in the microenvironment of the tumor-host interface that determine the individual tumor's malignant potential and in regulation of putative cancer stem or progenitor cells that represent plausible targets for cancer eradication.
- Subjects :
- Animals
Colorectal Neoplasms chemistry
Humans
Oncogene Proteins metabolism
beta Catenin metabolism
Cell Transformation, Neoplastic metabolism
Cell Transformation, Neoplastic pathology
Colorectal Neoplasms metabolism
Colorectal Neoplasms pathology
Oncogene Proteins physiology
Signal Transduction physiology
beta Catenin physiology
Subjects
Details
- Language :
- English
- ISSN :
- 1551-4005
- Volume :
- 4
- Issue :
- 11
- Database :
- MEDLINE
- Journal :
- Cell cycle (Georgetown, Tex.)
- Publication Type :
- Academic Journal
- Accession number :
- 16258275
- Full Text :
- https://doi.org/10.4161/cc.4.11.2129