Format

Send to

Choose Destination
See comment in PubMed Commons below
Rev Med Chir Soc Med Nat Iasi. 2012 Oct-Dec;116(4):1106-11.

Colon cancer at the molecular level--usefulness of epithelial-mesenchymal transition analysis.

Author information

1
University of Medicine and Pharmacy Grigore T Popa lasi, Faculty of Medicine.

Abstract

Colorectal cancer (CRC) is the third form of cancer in both men and women. In Romania, the incidence of CRC in 2000 is 17.74 %ooo, in 2002 becoming the second cause of death. We reviewed a series of studies that are related to colon cancer and studied the epithelial-mesenchymal transition at the front of tumor invasion (EMT). Cellular phenotypic changes characteristic of EMT can be induced by the absence of transition cofactor (p300) involved in cellular regulation. Loss of syndecan-l marker is associated with local tumor stage and metastasis. Modulators of protein kinase resistance was associated with changes in genes involved in EMT (including vimentin hyperexpression) and genes involved in invasion (N-cadherin) with a decrease expression of genes involved in epithelial cell adhesion (E-cadherin). Progression in colon cancer is characterized by activating mutations in Ras genes and tumor growth factor action. Vimentin expression associated with EMT initiates molecular program. One of the characteristics of EMT is the loss of E-cadherin. TGF-p (transforming growth factor beta) induces epithelial-mesenchymal transition in colon cancer cell lines with the microsatellite stability, inducing cell invasion and migration. EMT is a critical early event involved in invasion and metastasis of colorectal cancer, characterized by the presence of markers specific to each phenotype, epithelial or mesenchymal. Multiple biomarkers involved in the induction of EMT may represent future therapeutic target in the treatment of colonic neoplasia.

PMID:
23700897
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Loading ...
    Support Center