Consequently, to investigate the role of EGF in the modulation of urokinase protein/activity, cell types representative of well- and poorly differentiated colon cancer were examined for their sensitivity of expression to this growth factor.
Human colon cancer (Moser) cells produce and secrete epidermal growth factor (EGF) and respond to EGF via an autocrine/paracrine mode through the cell surface EGF receptor (EGFR).
Disrupting EGFR expression by expressing antisense EGFR RNA (through transfection with an appropriate antisense EGFR expression vector under metallothionein promoter control) downregulated the malignant behavior of human colon cancer Moser cells and blocked the ability of exogenous EGF in stimulating malignant cell behavior.
GEO is a well-differentiated colon cancer cell line that coexpresses the epidermal growth factor-like growth factors CRIPTO (CR), amphiregulin (AR), and transforming growth factor alpha (TGF-alpha).
The aims of this study were to characterize the endogenous epidermal growth factor (EGF)-like ligands expressed in two polarizing colon cancer cell lines, HCA-7 Colony 29 (HCA-7) and Caco-2, and to examine the effects of cell polarity on EGF receptor-mediated mitogenesis.
Data from in vitro studies utilizing colon cancer cell lines suggest that supplemental folic acid or its metabolite 5-methyltetrahydrofolate (5-MTF) attenuates the expression and activation of EGF-receptor (EGFR) as well as proliferation of cells.
Colon cancer-associated MS4A12 is a novel colon-specific component of store-operated Ca2+ (SOC) entry sensitizing cells for epidermal growth factor (EGF)-mediated effects on proliferation and chemotaxis.
Epidermal growth factor (EGF)-induced proliferation of colon cancer cells plays an important role in colon cancer progression and is mediated by loss of tumor suppressor FOXO3 activity.
Inhibition of AR prevented the epidermal growth factor (EGF) or fibroblast growth factor (FGF)-induced migration and invasion of human colon cancer (HT29; KM20) cells by >70% and also inhibited (>80%) the adhesion of the cancer cells to endothelial cells.
Receptor down-regulation is the most prominent regulatory system of EGF receptor (EGFR) signal attenuation and a critical target for therapy against colon cancer, which is highly dependent on the function of the EGFR.
At the level of matrix effectors implicated in colon cancer progression we report that pmAb is a potent inhibitor of constitute and EGF-mediated gene expression of certain matrix effectors, such as membrane-type 1 metalloproteinase (MT1-MMP), extracellular metalloproteinases inducer (EMMPRIN), urokinase plasminogen activator (uPA) and syndecan-4.
We also identified a subclass of proneural and neural glioblastoma with significantly better survival, and an EGF receptor-deregulated subclass of colon cancers.
Treatment of colon cancer cells (HT29, SW480 and Caco-2) with epidermal growth factor (EGF) caused increased expression of miR-21 and inhibition of AR prevented it.
TU-100 and some of its components and metabolites of these components inhibit tumor progression in two mouse models of colon cancer by blocking downstream pathways of EGF receptor activation.
Hydroxytyrosol (HT), a polyphenol of olive oil, downregulates epidermal growth factor (EGFR) expression and inhibits cell proliferation in colon cancer (CC) cells, with mechanisms similar to that activated by the EGFR inhibitor, cetuximab.