CD10-Equipped Melanoma Cells Acquire Highly Potent Tumorigenic Activity: A Plausible Explanation of Their Significance for a Poor Prognosis
نویسندگان
چکیده
CD10 has been widely used in cancer diagnosis. We previously demonstrated that its expression in melanoma increased with tumor progression and predicted poor patient survival. However, the mechanism by which CD10 promotes melanoma progression remains unclear. In order to elucidate the role of CD10 in melanoma, we established CD10-overexpressing A375 melanoma cells and performed DNA microarray and qRT-PCR analyses to identify changes in the gene expression profile. The microarray analysis revealed that up-regulated genes in CD10-A375 were mostly involved in cell proliferation, angiogenesis, and resistance to apoptosis; down-regulated genes mostly belonged to the categories associated with cell adhesion and migration. Accordingly, in functional experiments, CD10-A375 showed significantly greater cell proliferation in vitro and higher tumorigenicity in vivo; CD10 enzymatic inhibitors, thiorphan and phosphoramidon, significantly blocked the tumor growth of CD10-A375 in mice. In migration and invasion assays, CD10-A375 displayed lower migratory and invasive capacity than mock-A375. CD10 augmented melanoma cell resistance to apoptosis mediated by etoposide and gemcitabine. These findings indicate that CD10 may promote tumor progression by regulating the expression profiles of genes related to cell proliferation, angiogenesis, and resistance to apoptosis.
منابع مشابه
Immunohistochemical expression of CD10 in cutaneous basal and squamous cell carcinomas
Background: Non-melanoma skin cancer is the most common malignant tumor in humans. The role of ultraviolet radiation is well-known in the pathogenesis of basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). CD10 is a zinc-dependent metallopeptidase known as common acute lymphoblastic leukemia antigen (CALLA). Although CD10 expression has been investigated in some cutaneous tu...
متن کاملLipid Nanocapsules for Imatinib Delivery: Design, Optimization and Evaluation of Anticancer Activity Against Melanoma Cell Line
Lipid nanocapsules (LNCs) represent a stable, biocompatible and worthwhile drug delivery system, demonstrating significant potential as gene/drug delivery platforms for cancer therapy. Imatinib, a potent tyrosine kinase inhibitor, has revolutionized the therapy of malignancies resulting from abnormal tyrosine kinase activity. However, its Clinical effectiveness in cancer treatment is h...
متن کاملCD271 is an imperfect marker for melanoma initiating cells
Understanding the molecular and cellular processes underlying melanoma plasticity and heterogeneity is of paramount importance to improve the efficiency of current treatment and to overcome resistance to chemotherapy drugs. The notion of plasticity and heterogeneity implies the existence of melanoma cell populations with different phenotypic and tumorigenic properties. Using melanoma cell lines...
متن کاملMelanoma-Derived iPCCs Show Differential Tumorigenicity and Therapy Response
A point mutation in the BRAF gene, leading to a constitutively active form of the protein, is present in 45%-60% of patients and acts as a key driver in melanoma. Shortly after therapy induction, resistance to MAPK pathway-specific inhibitors develops, indicating that pathway inhibition is circumvented by epigenetic mechanisms. Here, we mimicked epigenetic modifications in melanoma cells by rep...
متن کاملThe Cell Survival of F10B16 Melanoma and 4T1 Breast Adenocarcinoma Irradiated to Gamma Radiation Using the MTT Assay Based on Two Different Calculation Methods
Background: Various MTT assay methods are proposed to obtain the cell sur- vival parameters.Objective: Determining the survival curve characteristics of two cancerous cells of interest based on a common and a novel MTT assay method after exposing them to ionizing radiation.Method: A common and a novel MTT assay method were used and compared for obtaining the F10B16 melanoma and 4T1 breast adeno...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره 11 شماره
صفحات -
تاریخ انتشار 2016