الفهرس 
Oral Squamous Cell Carcinoma (OSCC)
Apoptosis resistance and angiogenesis inductionOnly 14 pages are availabe for public view
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Abstract
Oral squamous cell carcinoma (OSCC) has a remarkable incidence worldwide, accounting for more than 90% of all malignant tumors of the head and neck. It is well established that microenvironment critically contribute to progression of OSCC. Among all stromal cells, fibroblasts constitute the most abundant cell type that undergo activation in cancer becoming cancer-associated fibroblasts (CAFs). CAFs attain a myofibroblastic phenotype that can be identified by α-smooth muscle actin (α-SMA) immunostaining. CAFs secrete a diverse group of growth factors, cytokines, chemokines, inflammatory mediators, adhesion proteins and proteases that all enhance cancer cell proliferation and subsequent progression. Cysteine cathepsins are family of lysosomal proteases with well-established wide spectrum of functions in nearly all tissue and cell types. Out of the 11 known cysteine cathepsins, cathepsin K (CTSK) is considered the most powerful collagenase that was first identified in osteoclasts as a bone resorption mediator. CTSK has important physiologic role in maintaining bone integrity and extracellular matrix (ECM) homeostasis. Also, CTSK is implicated in many disorders including bone, neurological, and cardiovascular diseases as well as cancer. CTSK expression is upregulated in a number of malignancies such as osteosarcoma, lung cancer, basal cell carcinoma, squamous cell carcinoma (SCC) of skin, and melanoma. Additionally, CTSK expression was evident in CAFs of tongue SCC, where it was correlated with increased tumor cell invasive potential. However, the contribution of CTSK to oral carcinogenesis is not fully elucidated as evidenced by paucity of published studies in the current literature.