Expression of integrin β6 enhances invasive behavior in oral squamous cell carcinoma

Ramos, Daniel M.; But, Maria; Regezi, Joseph A.; Schmidt, Brian L.; Atakilit, Amha; Dang, Dongmin; Ellis, Duncan; Jordan, Richard C.; Li, Xiaowu

doi:10.1016/s0945-053x(02)00002-1

Cited by 108 publications

(109 citation statements)

References 26 publications

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“…For example, increased integrin avb3 and a6b4 expression has been associated with increased cell invasion and metastasis in melanoma and breast carcinomas, respectively (Gehlsen et al, 1992;Nip et al, 1992;Mercurio et al, 2001;Ramos et al, 2002). Moreover, alterations in integrin activity have been shown to influence the angiogenic potential of endothelial cells.…”

Section: Src and Integrin In Cancermentioning

confidence: 99%

The interplay between Src and integrins in normal and tumor biology

2004

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Src family nonreceptor protein tyrosine kinases transduce signals that control normal cellular processes such as cell proliferation, adhesion and motility. Normally, cellular Src is held in an inactive state, but in several cancer types, abnormal events lead to elevated kinase activity of the protein and cause pleiotropic cellular responses inducing transformation and metastasis. A prerequisite of the ability of a cancer cell to undergo metastasis into distant tissues is to penetrate surrounding extracellular matrices. These processes are facilitated by the integrin family of cell adhesion molecules. As is the case with Src, altered integrin activity or substrate affinity can contribute to the neoplastic phenotype. Therefore, understanding the interplay between Src and integrin function has been of intense interest over the past few years. This review focuses on the role of Src and integrin signaling in normal cells and how this is deregulated in human cancer. We will identify the key players in the integrin-mediated signaling pathways involved in cell motility and apoptosis, such as FAK, paxillin and p130 CAS , and discuss how Src signaling affects the formation of focal adhesions and the extracellular matrix.

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Section: Src and Integrin In Cancermentioning

confidence: 99%

The interplay between Src and integrins in normal and tumor biology

2004

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“…Integrin a6 expression is also significantly upregulated in numerous carcinomas, including head and neck cancers and breast cancer (Garzino-Demo et al, 1998;Mercurio et al, 2001;Ramos et al, 2002). Integrin a6b4 expression enhances tumour cell invasiveness and metastasis, particularly in breast carcinomas (Mercurio et al, 2001;Ramos et al, 2002).…”

Section: Integrins Play Roles In Tumour Invasion and Metastasismentioning

confidence: 99%

“…Integrin a6b4 expression enhances tumour cell invasiveness and metastasis, particularly in breast carcinomas (Mercurio et al, 2001;Ramos et al, 2002). Thus, antagonists of these integrins may be useful to prevent the spread of tumour cells.…”

Section: Integrins Play Roles In Tumour Invasion and Metastasismentioning

confidence: 99%

Integrins: roles in cancer development and as treatment targets

2004

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The integrin family of cell adhesion proteins promotes the attachment and migration of cells on the surrounding extracellular matrix (ECM). Through signals transduced upon integrin ligation by ECM proteins or immunoglobulin superfamily molecules, this family of proteins plays key roles in regulating tumour growth and metastasis as well as tumour angiogenesis. Several integrins play key roles in promoting tumour angiogenesis and tumour metastasis. Antagonists of several integrins (a5b1, avb3 and avb5) are now under evaluation in clinical trials to determine their potential as therapeutics for cancer and other diseases.

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“…3,40 Given the diversity of ligands that a v integrins can bind, their upregulation in wound epidermis may be important for modulating keratinocyte motility over the complex matrix of the wound bed. Moreover, a v b 6 has been shown to regulate the expression of extracellular proteases, including matrix metalloprotease (MMP)-9, 101 MMP-3, 102 and uPA, 103 suggesting roles in ECM remodeling. Finally, as discussed below (in epidermal survival section), a v b 6 might promote cell survival and prevent keratinocytes from differentiating.…”

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confidence: 99%