Anoikis mechanisms

Frisch, Steven M.; Screaton, Robert A.

doi:10.1016/s0955-0674(00)00251-9

Cited by 1,259 publications

(1,075 citation statements)

References 69 publications

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“…Growing evidence indicates that collaborative pathways derived from these two signals are crucial in regulating a range of cell activities, such as proliferation, differentiation, apoptosis, adhesion, and migration [93][94][95][96].…”

Section: Versican Interaction With Epidermal Growth Factor Receptor (mentioning

confidence: 99%

The interaction of versican with its binding partners

et al. 2005

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Versican belongs to the family of the large aggregating chondroitin sulfate proteoglycans located primarily within the extracellular matrix (ECM). Versican, like other members of its family, has unique N-and C-terminal globular regions, each with multiple motifs. A large glycosaminoglycan-binding region lies between them. This review will begin by outlining these structures, in the context of ECM proteoglycans. The diverse binding partners afforded to versican by virtue of its modular design will then be examined. These include ECM components, such as hyaluronan, type I collagen, tenascin-R, fibulin-1, and -2, fibrillin-1, fibronectin, P-and L-selectins, and chemokines. Versican also binds to the cell surface proteins CD44, integrin β1, epidermal growth factor receptor, and P-selectin glycoprotein ligand-1. These multiple interactors play important roles in cell behaviour, and the roles of versican in modulating such processes are discussed.

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Section: Versican Interaction With Epidermal Growth Factor Receptor (mentioning

confidence: 99%

The interaction of versican with its binding partners

et al. 2005

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“…Taken together, these results strongly suggest that FZD10 overexpression induces Rac1 and JNK activation through phosphorylation of Dvl2 and Dvl3 proteins. Furthermore, as the Rac1 activation was indicated to be important for the inhibition of detachment-induced cell death (anoikis) (Frisch and Screaton, 2001;Cheng et al, 2004), we investigated the effect of FZD10 on anchorage-independent cell growth. When the cells were cultured in soft agar, the numbers of colonies in 1273/99-FZD10-1 and 1273/99-FZD10-2 were increased up to two-fold in comparison with the parental 1273/99 cells or those transfected with mock control (Mock1) (Figure 3g).…”

Section: Disruption Of Actin Cytoskeleton By Fzd10 Overexpressionmentioning

confidence: 99%

Activation of the non-canonical Dvl–Rac1–JNK pathway by Frizzled homologue 10 in human synovial sarcoma

et al. 2009

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We previously reported that Frizzled homologue 10 (FZD10), a member of the Wnt signal receptor family, was highly and specifically upregulated in synovial sarcoma and played critical roles in its cell survival and growth. We here report a possible molecular mechanism of the FZD10 signaling in synovial sarcoma cells. We found a significant enhancement of phosphorylation of the Dishevelled (Dvl)2/Dvl3 complex as well as activation of the Rac1-JNK cascade in synovial sarcoma cells in which FZD10 was overexpressed. Activation of the FZD10-Dvls-Rac1 pathway induced lamellipodia formation and enhanced anchorage-independent cell growth cells. FZD10 overexpression also caused the destruction of the actin cytoskeleton structure, probably through the downregulation of the RhoA activity. Our results have strongly implied that FZD10 transactivation causes the activation of the non-canonical Dvl-Rac1-JNK pathway and plays critical roles in the development/progression of synovial sarcomas.

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“…Normal mammary epithelial cells require attachment to the ECM to inhibit anoikis, which is defined as caspase-dependent cell death caused by ECM detachment. 17 It has become clear that tumor progression and metastasis require cancer cells to inhibit anoikis, oftentimes through alterations in intracellular signaling pathways. [18][19][20] Interestingly, previous studies have shown that ErbB2 and EGFR, which are hyperactivated in a substantial percentage of IBC patients, 21 can effectively antagonize the anoikis program to facilitate anchorage-independent growth.…”

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confidence: 99%

Anoikis evasion in inflammatory breast cancer cells is mediated by Bim-EL sequestration

et al. 2014

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Inflammatory breast cancer (IBC) is a rare and highly invasive type of breast cancer, and patients diagnosed with IBC often face a very poor prognosis. IBC is characterized by the lack of primary tumor formation and the rapid accumulation of cancerous epithelial cells in the dermal lymphatic vessels. Given that normal epithelial cells require attachment to the extracellular matrix (ECM) for survival, a comprehensive examination of the molecular mechanisms underlying IBC cell survival in the lymphatic vessels is of paramount importance to our understanding of IBC pathogenesis. Here we demonstrate that, in contrast to normal mammary epithelial cells, IBC cells evade ECM-detachment-induced apoptosis (anoikis). ErbB2 and EGFR knockdown in KPL-4 and SUM149 cells, respectively, causes decreased colony growth in soft agar and increased caspase activation following ECM detachment. ERK/MAPK signaling was found to operate downstream of ErbB2 and EGFR to protect cells from anoikis by facilitating the formation of a protein complex containing Bim-EL, LC8, and Beclin-1. This complex forms as a result of Bim-EL phosphorylation on serine 59, and thus Bim-EL cannot localize to the mitochondria and cause anoikis. These results reveal a novel mechanism that could be targeted with innovative therapeutics to induce anoikis in IBC cells.

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Anoikis mechanisms

Cited by 1,259 publications

References 69 publications

The interaction of versican with its binding partners

The interaction of versican with its binding partners

Activation of the non-canonical Dvl–Rac1–JNK pathway by Frizzled homologue 10 in human synovial sarcoma

Anoikis evasion in inflammatory breast cancer cells is mediated by Bim-EL sequestration

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