Matrix-directed regulation of pericellular proteolysis and tumor progression

Hornebeck, William; Emonard, Hervé; Monboisse, Jean-Claude; Bellon, Georges

doi:10.1016/s1044-579x(02)00026-3

Cited by 186 publications

(134 citation statements)

References 89 publications

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“…At the same time, elevated matrix metalloproteinase activity mediates increased collagen I degradation. Whether the latter results from an increase in collagenase and other MMPs or a decrease in tissue inhibitors of MMPs is still a matter of debate, but the end result is a looser, less organized collagen network (Hornebeck et al, 2002). Whereas some have suggested that a less dense collagen matrix facilitates vascular in-growth (Reed et al, 2005), studies of angiogenesis in most organs have demonstrated decreased capillary density with age (Rivard et al, 1999).…”

Section: Extracellular Matrixmentioning

confidence: 99%

Extracellular influences on tumour angiogenesis in the aged host

2008

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Whether tumours are epithelial or non-epithelial in origin, it is generally accepted that once they reach a certain size all solid tumours are dependent upon a vascular supply to provide nutrients. Accordingly, there is great interest in how the extracellular environment enhances or inhibits vascular growth. In this minireview, we will examine key extracellular components, their changes with ageing, and discuss how these alterations may influence the subsequent development of tumour vasculature in the aged host. Because of the tight correlation between advanced age and development of prostate cancer, we will use prostate cancer as the model throughout this review.

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Section: Extracellular Matrixmentioning

confidence: 99%

Extracellular influences on tumour angiogenesis in the aged host

2008

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“…In addition, most studies on integrin trafficking do not distinguish between ECM-bound and -unbound forms of the receptors. ECM remodeling has been shown to be critical to many cellular functions, including cell migration and invasion (Engelholm et al, 2003;Hocking and Chang, 2003;Hornebeck et al, 2002;Hotary et al, 2000;Sabeh et al, 2004). Therefore, coupling of ECM remodeling with integrin endocytosis/recycling may be an important feature of integrin trafficking.…”

Section: Introductionmentioning

confidence: 99%

Caveolin-1-dependent β1 integrin endocytosis is a critical regulator of fibronectin turnover

Shi

Sottile

2008

Journal of Cell Science

212

193

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“…Localized invasion and metastasis of EC results from several interdependent processes involving proteolytic enzymes (22). Among several cancer invasion-related characteristics, release of tumor-derived proteases is thought to break the basement membrane and extracellular matrix, thereby promoting cancer cell invasion into surrounding normal tissues and facilitating distant metastasis through lymphovascular channels (23).…”

Section: Discussionmentioning

confidence: 99%

Silencing of Cathepsin B suppresses the proliferation and invasion of endometrial cancer

et al. 2013

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Abstract. The molecular mechanism involved in the metastasis of endometrial cancer (EC) remains unclear. The lysosomal cysteine protease Cathepsin B has been implicated in the progression of various human tumors. In the present study, we assessed the expression of Cathepsin B and its functions in EC. Immunohistochemistry was used to examine Cathepsin B expression in 76 paraffin-embedded endometrial tumor tissues. Lentiviral packing short hairpin RNA (shRNA) was transfected into HEC-1A cells to build a stable Cathepsin B knockdown cell line. The cellular levels of Cathepsin B mRNA and protein were detected by real-time PCR and western immunoblotting. The functions of Cathepsin B in EC cells were measured by MTT, migration and invasion assays. In additon, tumorigenicity assays were established in nude mice to study tumor growth in vivo. The results of our study showed that Cathepsin B was overexpressed in EC tissues compared with normal endometrium and endometrial atypical hyperplasia. Depletion of Cathepsin B in vitro inhibited cell proliferation, migration and invasion. Tumor formation assays confirmed that suppression of Cathepsin B inhibited the proliferation potential of HEC-1A cells in vivo, demonstrated by lower proliferation rates. These results suggest that Cathepsin B may act as an oncogene in EC, with the potential to provide a new therapeutic target for treating endometrial malignancy.

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Matrix-directed regulation of pericellular proteolysis and tumor progression

Cited by 186 publications

References 89 publications

Extracellular influences on tumour angiogenesis in the aged host

Extracellular influences on tumour angiogenesis in the aged host

Caveolin-1-dependent β1 integrin endocytosis is a critical regulator of fibronectin turnover

Silencing of Cathepsin B suppresses the proliferation and invasion of endometrial cancer

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