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Example sentences for: anoikis
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PTEN is altered or deleted in many human cancers [ 7 8 9 10 ] . In-vitro, cells that are deficient in PTEN show elevated PI-3Kinase signaling [ 11 ] . Reintroduction of PTEN in a variety of cancer cells, including glioma, breast, bladder and ovarian cancer cells, causes G1 arrest, inhibits tumorigenesis, and promotes anoikis [ 12 13 14 ] . Mechanistically, Akt activity is decreased, cell motility is decreased, expression of two cyclin-dependent kinase inhibitors p27 and p21 is increased, cyclin D1 is down-regulated, Rb phosphorylation is inhibited, and signaling via Grb2/SOS is suppressed [ 11 15 ] . The link between PTEN and cell growth is underscored by genetic experiments in mice.
For example, mouse embryonal stem (ES) cells with homozygous deletion of the PTEN gene exhibit increased anchorage-independent growth as compared to normal ES cells [ 12 ] . Similarly, transfer of a wild type PTEN gene into anchorage-independent human glioblastoma cells (which lack functional PTEN), results in their greatly reduced ability to form colonies in soft agar [ 4 5 6 ] . The interpretation of these latter findings, however, is complicated by the strong anti-proliferative effects of PTEN even in monolayer culture, which is consistently observed when the wild type version of this gene is introduced into PTEN-negative tumor cells [ 4 6 7 8 9 10 18 33 ] . Moreover, in human glioma and breast cancer cell lines, the ectopic expression of wild type PTEN leads to anoikis, which is apoptosis initiated by the disruption of cell matrix-interactions [ 23 34 35 36 ] .
It should be noted that the fibroblast cells lines we used remain fully viable after detachment and transfer to suspension culture [ 31 43 ] . This is in contrast to most epithelial cells which undergo anoikis, i.e., apoptotic cell death after the disruption of cell-matrix interactions [ 45 ] . It is of interest that some anchorage-independent tumor cells, most of which are of epitheloid origin, become susceptible to anoikis after the introduction of exogenous PTEN [ 23 34 35 36 ] . These observations are in line with the established ability of PTEN to down-regulate the phosphatidylinositol 3-kinase (PI3-K)/PKB survival pathway [ 11 46 ] . The absence of anoikis in our two cell lines may reflect inherent cell type specific differences, i.e., the superior ability of fibroblasts to survive under suspension culture conditions.
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