In a paper published in this week's Online Early Edition of PNAS, researchers from the
The finding sheds new light upon the fundamental biology of hESCs - with their huge potential as a diverse therapeutic tool - but also suggests a new target for attacking cancer stem cells, which likely rely upon the same receptor and pathway to help spur their rampant, unwanted growth.
The research, led by principal investigator
"WNT signaling through FZD7 is necessary to maintain hESCs in an undifferentiated state," said Willert. "If we block FZD7 function, thus interfering with the WNT pathway, hESCs exit their undifferentiated and pluripotent state."
The researchers proved this by using an antibody-like protein that binds to FZD7, hindering its function. "Once FZD7 function is blocked with this FZD7-specific compound, hESCs are no longer able to receive the WNT signal essential to maintaining their undifferentiated state."
FZD7 is a so-called "onco-fetal protein," expressed only during embryonic development and by certain human tumors. Other studies have suggested that FZD7 may be a marker for cancer stem cells and play an important role in promoting tumor growth. If so, said Willert, disrupting FZD7 function in cancer cells is likely to interfere with their development and growth just as it does in hESCs.
Willert and colleagues, including co-author
Keywords for this news article include: Biomedical Engineering, Biomedicine,
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