Binding to EGF receptor of a laminin-5 EGF-like fragment liberated during MMP-dependent mammary gland involution

Schenk, Susann; Hintermann, Edith; Bilban, Martin; Koshikawa, Naohiko; Hojilla, Carlo V.; Khokha, Rama; Quaranta, Vito

doi:10.1083/jcb.200208145

Cited by 273 publications

(240 citation statements)

References 57 publications

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“…Waterman and coworkers demonstrated that by in vivo model of human skin keratinocytes, the binding of laminin-332 to a6b4 integrin associated and drove tumorgenesis and invasion thorough PI3K activation in skin squamous cell carcinoma (Waterman et al, 2007). Furthermore, the interaction between laminin-332 g2 chain III domain and EGFR has been suggested to have a role in PI3K activation via the action of FYN kinase (Schenk et al, 2003;Guo et al, 2006;Marinkovich, 2007). Briefly, the interaction of laminin-332 with a6b4 integrin and EGFR is involved in promoting PI3K activation and tumour invasion.…”

Section: Discussionmentioning

confidence: 99%

Laminin-332 promotes the invasion of oesophageal squamous cell carcinoma via PI3K activation

et al. 2008

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Laminin-332 is major component of epithelial basement membrane, and has an important role in cell migration and tumour invasion. Recently, the phosphatidylinositol 3-kinase (PI3K) activation induced by laminin-332 during carcinogenesis or tumour invasion has been highlighted in skin squamous cell carcinoma. The expression of laminin-332 in 126 resected oesophageal squamous cell carcinoma (ESCC) specimens was immunohistochemically examined to determine its associations with the clinicopathological characteristics, and the effect of laminin-332 on the invasiveness and the PI3K activation was assessed by in vitro experiments using ESCC cell lines (ESCCs). Sections with immunostaining signals in 430% cancer cells, which were observed in 55 of 126 cases, were judged to be positive for laminin-332. The positivity was significantly correlated with pTNM stage and poor prognosis. Inactivation of the PI3K pathway by laminin-332 blocking antibody suppressed the invasiveness of TE8 cell line, which secreted laminin-332 at high level and had high PI3K activity. The addition of the purified laminin-332 activated the PI3K pathway and increased the invasiveness of TE11 cell line, which secreted laminin-332 at lower level and had low PI3K activity. The deactivation of PI3K pathway using the PI3K inhibitor decreased the invasiveness of ESCCs and the secretion of laminin-332 in vitro. The expression of laminin-332 was one of the prognostic factors of ESCC. Laminin-332 could provide the autocrine positive-feedback loop through PI3K activation, contributing the invasive ability. Therefore, the inhibitor of PI3K pathway might be useful as the anticancer therapies for ESCC.

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Section: Discussionmentioning

confidence: 99%

Laminin-332 promotes the invasion of oesophageal squamous cell carcinoma via PI3K activation

et al. 2008

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“…For example, the g2 subunit DIII fragment of laminin-5 can bind to the cell surface of MDA-MB-231 breast cancer cells and upregulate the expression of MMP-2 and -9 resulting in an increase migratory activity (Schenk et al, 2003). The involvement of these two mechanisms in radiation enhancement of cancer cell invasion deserves to be tested in subsequent studies.…”

Section: Discussionmentioning

confidence: 99%

In vitro irradiation of basement membrane enhances the invasiveness of breast cancer cells

et al. 2007

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Following removal of the primary breast tumour by conservative surgery, patients may still have additional malignant foci scattered throughout the breast. Radiation treatments are not designed to eliminate all these residual cancer cells. Rather, the radiation dose is calculated to optimise long-term results with minimal complications. In a tumour, cancer cells are surrounded by a basement membrane, which plays an important role in the regulation of gene expression. Using an invasion chamber, we have shown that irradiation before cell plating of a reconstituted basement membrane (Matrigel; Becton Dickinson, Bedford, MA, USA) increased the invasiveness of the breast cancer cells MDA-MB-231. This radiation enhancement of invasion was associated with the upregulation of the pro-invasive gene matrix metalloproteinase (MMP)-2. The expression of membrane type 1 matrix metalloproteinase (MT1-MMP) and tissue inhibitor of metalloproteinase-2 (TIMP), which are required to activate the MMP-2, were also increased. Confirming the role of MMP-2 and MT1-MMP, radiation enhancement of cancer cell invasion was prevented by an MMP-2 inhibitor and an anti-MT1-MMP antibody. This study also demonstrated that radiation can potentially enhance the invasion ability by inducing the release of pro-invasive factors stored in the Matrigel. Conversely, no enhancement of invasiveness was observed with the low metastatic cell line MCF-7. This lack of invasiveness correlated with the absence of the MMP-2 activator MT1-MMP in the MCF-7 cells. Radiotherapy is an efficient modality to treat breast cancer which could be further improved by inhibiting the pro-invasive gene upregulated by radiation.

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“…For example, cleavage of CD44 by MMP-14 results in increased motility in different cancer cell lines and mutation of the putative MMP-14 cleavage site in CD44 inhibits migration (Kajita et al, 2001). Also, MMP-2 and MMP-14 cleavage of ECM components such as laminin-5 reveal cryptic sites that act as chemotactic factors that trigger invasion as well as activate signaling via the EGF receptor (Giannelli et al, 1997;Schenk et al, 2003). The acquisition of mesenchymal characteristics by epithelial cells represents a key step in epithelial tumour progression.…”

Section: Cell Dissociationmentioning

confidence: 99%

Matrix metalloproteinases and their tissue inhibitors direct cell fate during cancer development

2003

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Matrix metalloproteinases (MMPs) were initially recognised for their extracellular matrix (ECM)-degrading capability during tissue remodelling. Their importance was further highlighted by their role in metastasis. Clinical trials have since evaluated the potential of MMP inhibitors as anticancer therapeutics, but without success. These initial studies point to the complex, multifunctional capacity of MMPs in cancer as shown by their function, not only as strident mediators of advanced malignancies, but also as effectors of early stage tumorigenesis. Research now shows that MMPs, and their tissue inhibitors, affect tumour initiation and growth through loss of cell adhesion, evasion of apoptosis, and deregulation of cell division. The extracellular nature of the metalloproteinase axis situates it as a master regulator of cell fate.

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Binding to EGF receptor of a laminin-5 EGF-like fragment liberated during MMP-dependent mammary gland involution

Cited by 273 publications

References 57 publications

Laminin-332 promotes the invasion of oesophageal squamous cell carcinoma via PI3K activation

Laminin-332 promotes the invasion of oesophageal squamous cell carcinoma via PI3K activation

In vitro irradiation of basement membrane enhances the invasiveness of breast cancer cells

Matrix metalloproteinases and their tissue inhibitors direct cell fate during cancer development

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