In the present study, monoclonal tongue squamous carcinoma cells were cultured after being monoclonally cultured (4) found that 100 CD133+ cells could lead to tumourigenesis in NOD/SCID mice

In the present study, monoclonal tongue squamous carcinoma cells were cultured after being monoclonally cultured (4) found that 100 CD133+ cells could lead to tumourigenesis in NOD/SCID mice. have been identified in numerous types of malignancies (3C5). As a result, Rabbit polyclonal to RABEPK increasing attention has been focused on cancer stem cells in oncological research. However, there have been few reports on oral and maxillofacial malignant tumours. Cluster of differentiation 133 (CD133; formerly known MM-102 TFA as AC133) is usually a highly-conserved antigen that is the human homologue of mouse Prominin-1, which was initially identified as a 5-transmembrane cell surface glycoprotein, and was classified as a marker for primitive haematopoietic and neural stem cells. CD133 is also considered a universal marker of organ-specific stem cells and tumour-initiating cells. CD133 protein plays an important role in supporting tumour growth (6,7). In addition, CD133+ cells are involved in tumourigenesis, invasion, metastasis, drug resistance and disease relapse (8). CD133 is usually detectable in a range of solid tumours, but there has been little research on its role in oral and maxillofacial tumours. Based on a previous study around the characterisation of cancer stem cells, CD133 has been identified as a common marker for cancer stem cells (9). It is therefore reasonable to suspect that the CD133 antigen is usually a marker for cancer stem cells associated with tongue squamous carcinoma. The purpose of the present study was to determine whether CD133 is usually a surface marker of tongue squamous carcinoma stem cells. In this study, immunomagnetic beads were used to select and purify CD133+ tumour cells, which were then cultured. The proliferative ability of these cells was observed (3) first verified the presence MM-102 TFA of tumour stem cells in solid tumours by identifying tumour stem cells with the characteristic marker LinCESA+/CD44+/CD24C/low in a breast carcinoma NOD/SCID mouse model. Recently, Singh (4) identified CD133+ as a cell-surface marker in brain tumours. A study by Jordan (13) also exhibited the oncogenicity of CD133+ cells, which further supports the hypothesis of tumour stem cells. In the present study, the isolation and characterisation of a highly tumourigenic subpopulation of cells were described in human tongue squamous carcinoma. We believe that this is the first description of the isolation of malignant progenitors from human tongue squamous carcinoma. Over the past several years, CD133 has been identified as a cancer stem cell marker, including stem cells for cancer of adult brain, prostatic carcinoma, colon carcinoma and liver malignancy (5,14C17). Five individual criteria have been established for cancer stem cells: i) The cells can self-renew; ii) they are part of a small minority of the total tumour cell populace; iii) they present a reproducible tumour phenotype; iv) they are capable of multipotent differentiation into non-tumourigenic cells; and v) they carry distinct cell surface antigenic phenotypes, permitting consistent isolation MM-102 TFA (18,19). CD133+ cancer stem cells are capable of unlimited self-renewal (20). Therefore, we hypothesized that cancer stem cells may exist in tongue squamous carcinoma. Further investigations will be performed to determine whether the CD133 antigen is usually a surface marker of tumour stem cells, and to assess the biological activity and proliferation state of CD133+ cells in the human tongue squamous carcinoma Tca8113 cell line. Malignant tumours are capable of unlimited self-renewal and heterogeneity (21). In the present study, monoclonal tongue squamous carcinoma cells were cultured after being monoclonally cultured (4) found that 100 CD133+ cells could lead to tumourigenesis in NOD/SCID mice. However, transplantation of 50,000C100,000 CD133C cells did not lead to tumourigenesis. A study by Jordan (13) further confirmed the tumourigenesis of CD133+ cells. O’Brien (5) used tumours from patients with colon cancer to inject CD133 antibodies into NOD/SCD mice, and the result demonstrated that CD133+ had a strong tumourigenic ability. The CD133+ tumour cells in the NOD/SCID mice were again transplanted into new NOD/SCID mice, and the result demonstrated that this newly formed tumours had a similar phenotypic heterogeneity as the original tumours. The present study also used NOD/SCID mice. Suspensions of CD133+, CD133C and unsorted cells (5105/-2.5108/ml) from the tongue squamous cell line were subcutaneously injected into the mice using a syringe (after disinfection). After 2 months, the subcutaneous tumours were exposed following sacrifice of the NOD/SCID mice, and the tumours generated from the CD133+ cells were significantly larger than those.