Project description:To identify the genes that are regulated during passaging of the parental mouse Dunn osteosarcoma cells with low metastatic potential and Dunn-derived LM8 cells with increased metastatic potential, we performed global gene expression profiling in early and late passage cells.
Project description:To identify the genes that are regulated during passaging of the parental osteosarcoma cells SAOS-2 and HOS with low metastatic potential, and SAOS-2-derived LM5 cells and Ki-ras transformed HOS cells (143B) with increased metastatic potential, we performed global gene expression profiling in early and late passage cells.
Project description:To identify chromosomal aberrations during passaging of parental SAOS-2 osteosarcoma cells with low metastatic potential and of SAOS-2-derived LM5 cells with increased metastatic potential
Project description:Syndecan-2 was found to act as a tumor suppressor in osteosarcoma and to mediate the apoptotic response to cytotoxic agents. To determine new mechanisms that control cell survival and apoptosis in osteosarcoma cells, we aim to show target genes that are involved downstream of this proteoglycan during apoptosis induction. We aim to compare the modifications induced by syndecan-2 overexpression in two different human osteosarcoma cell lines using a lentiviral vector coding the human syndecan-2. Syndecan-2 lentiviral vector (SY) and control empty lentiviral vector (VV) were transducted in two different human osteosarcoma cell lines in a dye-swap experiment.
Project description:Syndecan-2 was found to act as a tumor suppressor in osteosarcoma and to mediate the apoptotic response to cytotoxic agents. To determine new mechanisms that control cell survival and apoptosis in osteosarcoma cells, we aim to show target genes that are involved downstream of this proteoglycan during apoptosis induction. We aim to compare the modifications induced by syndecan-2 overexpression in two different human osteosarcoma cell lines using a lentiviral vector coding the human syndecan-2.