Project description:Several novel potential oncogenic and tumor suppressor miRNAs were identified by using the appropriate controls for stem cells. Expression profiles for human miRNAs in six samples were generated. The Agilent platform GPL7731 was used to analyze six RNA samples: CD133- human NPC, CD133+ human NPC, CD133- B4 glioma, CD133+ B4 Glioma, CD133+ NCH441 glioma, CD133+ NCH644 glioma
Project description:Given the very substantial heterogeneity of most human cancers, it is likely that most cancer therapeutics will be active in only a small fraction of any population of patients. As such, the development of new therapeutics, coupled with methods to match a therapy with the individual patient, will be critical to achieving significant gains in disease outcome. One such opportunity is the use of expression signatures to identify key oncogenic phenotypes that can serve not only as biomarkers but also as a means of identifying therapeutic compounds that might specifically target these phenotypes. Given the potential importance of targeting tumors exhibiting a stem-like phenotype, we have developed an expression signature that reflects common biological aspects of various stem-like characteristics. The Consensus Stemness Ranking (CSR) signature is upregulated in cancer stem cell enriched samples, at advanced tumor stages and is associated with poor prognosis in multiple cancer types. Using two independent computational approaches we utilized the CSR signature to identify clinically useful compounds that could target the CSR phenotype. In vitro assays confirmed selectivity of several predicted compounds including topoisomerase inhibitors and resveratrol towards breast cancer cell lines that exhibit a high-CSR phenotype. Importantly, the CSR signature could predict clinical response of breast cancer patients to a neoadjuvant regimen that included a CSR-specific agent. Collectively, these results suggest therapeutic opportunities to target the CSR phenotype in a relevant cohort of cancer patients. CD133+ and CD133- cells were separated from two glioma xenograft tumors. Both CD133+ and CD133- glioma cells were cultured in serum-free media for 48 hours in the presence of absence of laminin.
Project description:To identify the gene expression signature associated with CD133, the well-known stem cell markers, three gastric cancer cell lines were obtained (KATO-III, SNU201 and SNU601). Cultured gastric cancer celllines were sorted into CD133+ and CD133- population by FACS sorting and microarray-based gene expression profiling was performed.
Project description:MEFs were grown from WT and PDPN-deficient mouse embryos and gene expression was analyzed. The aim was to determine whether a lack of PDPN caused significant global changes in gene expression in primary fibroblasts. Here, we performed a microarray on WT and PDPN-deficient mouse embryonic fibroblasts to determine whether there were signficiant underlying changes in gene expression. Two replicates each of WT and PDPN KO MEFs from C57BL6/J mice
Project description:Podoplanin, a transmembrane sialomucin-like glycoprotein, is now widely used as a marker for lymphatic endothelial cells and fibroblastic reticular cells in lymphoid organs, but its study in nasopharyngeal carcinoma (NPC) is still limited. The aims of this study were t characterize the role of PDPN in NPC. Our results showed that PDPN was expressed in most TW01 NPC cells. PDPN knockdown by siRNA decreased NPC cell proliferation, migration, and invasion. Knocking down PDPN results in suppression of NPC cell proliferation, migration, and invasion. PDPN may serve as a potential chemotherapeutic target for NPC treatment in the future.
Project description:Gene expression signature of EpCAMlow/PDPN+ and EpCAMhigh/PDPN- cancer cells in engineered human NSCLC HSAEC_4T53RD mouse xenograft model.
Project description:MEFs were grown from WT and PDPN-deficient mouse embryos and gene expression was analyzed. The aim was to determine whether a lack of PDPN caused significant global changes in gene expression in primary fibroblasts. Here, we performed a microarray on WT and PDPN-deficient mouse embryonic fibroblasts to determine whether there were signficiant underlying changes in gene expression.