Abstract
The Wnt and Notch signalling pathways play major roles in mammary gland development and tumourigenesis. During development, these pathways have opposing effects. However, in a recent paper Ayyanan and coworkers show that expression of Wnt1 is sufficient to transform primary human mammary epithelial cells, and that this is in part due to activation of the Notch pathway. This indicates that during tumourigenesis the two pathways cooperate. Here we ask why activation of Wnt signalling alone is sufficient to cause transformation; whether there is evidence for inhibitory crosstalk between the pathways during tumourigenesis; and whether cooperation between these pathways occurs in other forms of cancer.
Highlights
We ask is there evidence that Wnt signalling can regulate all of these cellular properties simultaneously? Wnt signalling is known to affect cell proliferation and growth in colorectal cancer by stimulating expression of CyclinD1 and c-myc, respectively [3]
The expression of Wnt1 in human mammary epithelial cells (HMECs) may increase the number of stem cells within this cell population; interestingly, stem cells exhibit resistance to apoptosis and failure to senesce similar to those in transformed cells
It is clear that Wnt signalling regulates many cellular properties at once, unlike classical oncogenes, which may explain its ability to HMEC = human mammary epithelial cell
Summary
We ask is there evidence that Wnt signalling can regulate all of these cellular properties simultaneously? Wnt signalling is known to affect cell proliferation and growth in colorectal cancer by stimulating expression of CyclinD1 and c-myc, respectively [3]. Wnt signalling is known to affect cell proliferation and growth in colorectal cancer by stimulating expression of CyclinD1 and c-myc, respectively [3]. The expression of Wnt1 in HMECs may increase the number of stem cells within this cell population; interestingly, stem cells exhibit resistance to apoptosis and failure to senesce similar to those in transformed cells.
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