Archived Comments for:
Nestin positively regulates the Wnt/β-catenin pathway and the proliferation, survival and invasiveness of breast cancer stem cells
Nestin-Wnt-EMT axis is observed also in breast non-CSCs much the same in CSCs?
Go Yoshida, Tokyo Medical and Dental University
18 December 2014
I am not sure whether or not the positive regulation of canonical Wnt pathway by Nestin is limited exclusively to the breast cancer stem cell (CD44high/CD24low) population. The authors only investigated in this article that Nestin knockdown in breast CSCs resulted in attenuated Wnt signal activity and subsequently caused mesenchymal-epithelial transition (MET). That is why it remains to be known whether or not Nestin overexpression in breast CSCs is responsible for up-regulation of c-Myc via increased nuclear translocation of beta-catenin in CSCs, thereby inducing EMT. When that should be the case, Nestin-Wnt-EMT axis in breast non-CSCs might provide ectopic CSCs.
Nestin-Wnt-EMT axis is observed also in breast non-CSCs much the same in CSCs?
18 December 2014
I am not sure whether or not the positive regulation of canonical Wnt pathway by Nestin is limited exclusively to the breast cancer stem cell (CD44high/CD24low) population. The authors only investigated in this article that Nestin knockdown in breast CSCs resulted in attenuated Wnt signal activity and subsequently caused mesenchymal-epithelial transition (MET). That is why it remains to be known whether or not Nestin overexpression in breast CSCs is responsible for up-regulation of c-Myc via increased nuclear translocation of beta-catenin in CSCs, thereby inducing EMT. When that should be the case, Nestin-Wnt-EMT axis in breast non-CSCs might provide ectopic CSCs.
Competing interests
There are no competing interests.