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OSCC Cells (oscc + cell)

Distribution by Scientific Domains
Medical Sciences100%

Terms modified by OSCC Cells

  • oscc cell line
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    Selected Abstracts

    Tumor-stromal crosstalk in invasion of oral squamous cell carcinoma: a pivotal role of CCL7

    INTERNATIONAL JOURNAL OF CANCER, Issue 2 2010
    Da-Woon Jung
    Abstract Recent studies have shown that stromal fibroblasts have a more profound influence on the initiation and progression of carcinoma than was previously appreciated. This study aimed at investigating the reciprocal relationship between cancer cells and their associated fibroblasts at both the molecular and cellular level in oral squamous cell carcinoma (OSCC). To identify key molecular regulators expressed by carcinoma-associated fibroblasts (CAF) that promote cancer cell invasion, microarrays were performed by comparing cocultured OSCC cells and CAF with monoculture controls. Microarray and real-time PCR analysis identified marked upregulation of the chemokine (C-C motif) ligand 7 (CCL7) in cocultured CAF. ELISA showed an elevated level of CCL7 secretion from CAF stimulated by coculture with OSCC cells. CCL7 promoted the invasion and migration of OSCC cells, and the invasiveness was inhibited by treatment with CCL7 neutralizing antibody. OSCC cells were shown to express CCR1, CCR2 and CCR3, receptors for CCL7, by RT-PCR. In addition, treatment with anti-CCR1 or anti-CCR3 antibody inhibited CCL7-induced OSCC cell migration, implicating that CCL7 promotes cancer cell migration through CCR1 and CCR3 on OSCC cells. Cytokine antibody array analysis of the supernatant from OSCC cell culture revealed that interleukin-1, was an inducer of CCL7 secretion by CAF. This study confirms the reciprocal relationship of the molecular crosstalk regulating the invasion of OSCC and describes new potential targets for future therapy. [source]

    Nm23-H1 expression of metastatic tumors in the lymph nodes is a prognostic indicator of oral squamous cell carcinoma

    INTERNATIONAL JOURNAL OF CANCER, Issue 2 2008
    Yi-Fen Wang
    Abstract We recently reported that low Nm23-H1 expression of primary oral squamous cell carcinoma (OSCC) was correlated with the occurrence of lymphatic metastasis. However, little is known about whether Nm23-H1 level of metastatic tumors in the cervical lymph nodes is reduced in comparison with primary oral cancers and its significance for patients' prognosis. By immunohistochemistry, we analyzed the Nm23-H1 expression in 52 pairs of OSCC specimens from primary oral cancers and their metastatic lymph nodes. Western blot analysis further confirmed the immunohistochemical interpretation. To verify the effects of Nm23-H1 on cell migration and invasion, we established several stable clones derived from a human OSCC cell line (SAS) by knockdown and overexpression. Wound-healing closure, transwell migration and invasion assays were performed to determine cell motility, migratory and invasive activities. Western blot analysis was carried out to evaluate cyclin A expression of OSCC cells with the altered Nm23-H1 levels following knockdown and overexpression. By immunohistochemistry, Nm23-H1 expression of metastatic lymph nodes was significantly lower than that of their primary oral cancers, supporting a role of Nm23-H1 in metastasis suppression. Negative Nm23-H1 interpretation of OSCC specimens, in either primary oral cancers or metastatic lymph nodes, indicated a poor survival outcome of patients. On the basis of in vitro studies of Nm23-H1 knockdown and overexpression, we demonstrated an inverse correlation between Nm23-H1 expression and the invasiveness of OSCC cells. Moreover, we observed the concomitant reduction in Nm23-H1 and cyclin A levels of metastatic tumors in both results of in vitro OSCC cells and ex vivo tumor specimens. © 2007 Wiley-Liss, Inc. [source]

    The involvement of hypoxia-inducible factor-1, in the susceptibility to ,-rays and chemotherapeutic drugs of oral squamous cell carcinoma cells

    INTERNATIONAL JOURNAL OF CANCER, Issue 2 2007
    Eri Sasabe
    Abstract The transcription factor hypoxia-inducible factor-1, (HIF-1,) is the key regulator that controls the hypoxic response of mammalian cells. The overexpression of HIF-1, has been demonstrated in many human tumors. However, the role of HIF-1, in the therapeutic efficacy of chemotherapy and radiotherapy in cancer cells is poorly understood. In this study, we investigated the influence of HIF-1, expression on the susceptibility of oral squamous cell carcinoma (OSCC) cells to chemotherapeutic drugs (cis -diamminedichloroplatinum and 5-fluorouracil) and ,-rays. Treatment with chemotherapeutic drugs and ,-rays enhanced the expression and nuclear translocation of HIF-1,, and the susceptibility of OSCC cells to the drugs and ,-rays was negatively correlated with the expression level of HIF-1, protein. The overexpression of HIF-1, induced OSCC cells to become more resistant to the anticancer agents, and down-regulation of HIF-1, expression by small interfering RNA enhanced the susceptibility of OSCC cells to them. In the HIF-1,-knockdown OSCC cells, the expression of P-glycoprotein, heme oxygenase-1, manganese-superoxide dismutase and ceruloplasmin were downregulated and the intracellular levels of chemotherapeutic drugs and reactive oxygen species were sustained at higher levels after the treatment with the anticancer agents. These results suggest that enhanced HIF-1, expression is related to the resistance of tumor cells to chemo- and radio-therapy and that HIF-1, is an effective therapeutic target for cancer treatment. © 2006 Wiley-Liss, Inc. [source]

    Nuclear STK15 expression is associated with aggressive behaviour of oral carcinoma cells in vivo and in vitro,

    THE JOURNAL OF PATHOLOGY, Issue 1 2010
    Shou-Yen Kao
    Abstract Oral squamous cell carcinoma (OSCC) is one of the most commonly diagnosed cancers worldwide. Chromosome 20q is a hotspot for gene amplification in OSCC and the serine/threonine kinase STK15 (also named Aurora-A) maps to 20q13. The amplification and over-expression of STK15 is common in neoplasia but the functional and clinical impact of STK15 in OSCC remains poorly understood. STK15 copy number is amplified in 12% of OSCCs and nuclear STK15 protein expression increases with tumour progression. In vivo elevated nuclear STK15 protein expression is significantly associated with the worse prognosis of OSCC patients. The combination of high nuclear STK15 and Ki-67 expression has a 2.55-fold hazard for cancer-associated mortality. In vitro knockdown of STK15 reduced the oncogenic phenotypes of OECM-1 cells. Injection of lentivirus carrying shRNA vectors against STK15 significantly reduced the growth of SAS xenografts on nude mice. Knockdown of STK15 also induced autophagy and apoptosis of OSCC cells. Our data provide evidence that STK15 is oncogenic for OSCC and that its nuclear expression is a predictor of clinical behaviour. Knockdown of STK15 could be a potential therapeutic option in OSCC and other tumours. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source]