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Review |
From the Department of Pathology,*
University ofEdinburgh, Edinburgh, and the Department of Pathology andMicrobiology,
Division of Histopathology,Bristol Royal Infirmary, Bristol, United Kingdom
Abstract
An important role for ß-catenin pathways in colorectal
carcinogenesis was first suggested by the protein’s association with
adenomatous polyposis coli (APC) protein, and by evidence of
dysregulation of ß-catenin protein expression at all stages of the
adenoma-carcinoma sequence. Recent studies have,
however, shown that yet more components of
colorectal carcinogenesis are linked to ß-catenin pathways.
Pro-oncogenic factors that also release ß-catenin from the adherens
complex and/or encourage translocation to the nucleus include
ras, epidermal growth factor (EGF),
c-erbB-2, PKC-ßII, MUC1, and
PPAR-
, whereas anti-oncogenic factors that also inhibit
nuclear ß-catenin signaling include transforming growth factor
(TGF)-ß, retinoic acid, and vitamin D. Association of
nuclear ß-catenin with the T cell factor (TCF)/lymphoid enhancer
factor (LEF) family of transcription factors promotes the expression of
several compounds that have important roles in the development and
progression of colorectal carcinoma, namely:
c-myc, cyclin D1, gastrin,
cyclooxygenase (COX)-2, matrix metalloproteinase
(MMP)-7, urokinase-type plasminogen activator receptor
(aPAR), CD44 proteins, and P-glycoprotein.
Finally, genetic aberrations of several components of the
ß-catenin pathways, eg, Frizzled (Frz),
AXIN, and TCF-4, may potentially contribute to
colorectal carcinogenesis. In discussing the above
interactions, this review demonstrates that ß-catenin
represents a key molecule in the development of colorectal
carcinoma.
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