| Original language | English (US) |
|---|---|
| Pages (from-to) | 15 |
| Number of pages | 1 |
| Journal | Cell Cycle |
| Volume | 10 |
| Issue number | 1 |
| DOIs |
|
| State | Published - Jan 1 2011 |
ASJC Scopus subject areas
- Molecular Biology
- Developmental Biology
- Cell Biology
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Function following form : Functional differentiation of mammary epithelial cells requires laminin-induced polarization of PI3-kinase. / Radisky, Derek C.
In: Cell Cycle, Vol. 10, No. 1, 01.01.2011, p. 15.Research output: Contribution to journal › Comment/debate › peer-review
}
TY - JOUR
T1 - Function following form
T2 - Functional differentiation of mammary epithelial cells requires laminin-induced polarization of PI3-kinase
AU - Radisky, Derek C.
N1 - Funding Information: surface where it could be more effectively differential response of normal and cancer activated by soluble hormone.8 in the study, cells to ECM and soluble signaling factors, Xu et al. identified phosphoinositide-3 kinase and better understanding of why the former (Pi3K) as the key signaling molecule linking respond by arresting growth and functionally LN1 and prolactin signaling pathways. They differentiating, while the latter continue to found that when cultured in plates coated proliferate and fail to differentiate. The elegant with polyHEMA, which prevents adhesion to cell culture system described by Xu et al. their the plastic substratum, MEC form unpolarized recent study should make these questions cell aggregates that show only transient acti-much more tractable. vation of STAT5 and no stimulation of β-casein gene expression in response to prolactin. By Acknowledgements contrast, they found that LN1-induced struc-D.C.R. is supported by National institutes of tural polarization of the MEC was associated Health Grant CA122086 and by support from with functional activation of the prolactin sig-the Mayo Clinic Breast Cancer Specialized naling pathway: sustained activation of STAT5 Program of Research Excellence (SPORE) Grant and stimulation of β-casein gene expression. CA116201 (to James ingle). They evaluated Pi3K as a potential mediator of this effect due to its role as a key mediator of integrin-induced signaling pathways, and found that inhibition of Pi3K blocked LN1- mediated activation of prolactin signaling and also blocked LN1-mediated activation of Rac1, a key downstream effector of Pi3K which was previously found to be crucial for STAT5 activa- tion and functional differentiation of MECs.9
PY - 2011/1/1
Y1 - 2011/1/1
UR - http://www.scopus.com/inward/record.url?scp=78650826005&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=78650826005&partnerID=8YFLogxK
U2 - 10.4161/cc.10.1.14218
DO - 10.4161/cc.10.1.14218
M3 - Comment/debate
C2 - 21200145
AN - SCOPUS:78650826005
SN - 1538-4101
VL - 10
SP - 15
JO - Cell Cycle
JF - Cell Cycle
IS - 1
ER -