Example sentences for: anoikis

How can you use “anoikis” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • 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.

  • 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 ] .

  • 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.

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