Project description:Inhibition of miR-361-3p by locked nucleic acid (LNA)/DNA antisense oligonucleotide markedly suppressed the growth of GFP-SAS cells. We explored the target genes of miR-361-3p in GFP-SAS cells using microarray analysis.
Project description:Knockdown of AURKA by siAURKA and treatment with MLN8237 markedly inhibit the growth of GFP-SAS cells. We investigated the molecular mechanisms of siAURKA and MLN8237 using the Affymetrix GeneAtlasTM System. Using the Affymetrix GeneAtlas System, we compared gene expression profiles of GFP-SAS cells treated with siAURKA, siNon-target (siNT), MLN8237, or DMSO.
Project description:Knockdown of AURKA by siAURKA and treatment with MLN8237 markedly inhibit the growth of GFP-SAS cells. We investigated the molecular mechanisms of siAURKA and MLN8237 using the Affymetrix GeneAtlasTM System.
Project description:To examine the role of hepatpcyte growth factor activator inhibitor type 1 (HAI-1) in cancer, we analyzed effect of HAI-1 silencing on gene expression profiles of human oral squamous cell carcinoma cell line, SAS. We used short hairpin RNA (shRNA) directed against HAI-1 mRNA. We constructed retroviral vectors which showed stable and significant silencing effects on HAI-1 genes of SAS. Microarray data of the expression profiles of duplicated experiments of HAI-1-knockdown SAS with that from the control cell are shown.
Project description:Knockdown of Akt1 markedly inhibited the growth of GFP-SAS cells. We investigated the molecular mechanisms of the growth inhibitory effect by siAkt1 using Affymetrix GeneAtlasTM System. Using Affymetrix GeneAtlas System, we determined the gene expression profiles of GFP-SAS cells treated with siAkt1 or non-targeting siRNA (siNT).
Project description:Knockdown of Akt1 markedly inhibited the growth of GFP-SAS cells. We investigated the molecular mechanisms of the growth inhibitory effect by siAkt1 using Affymetrix GeneAtlasTM System.
Project description:Transcriptional profiling of SAS cells transfected with pLKO.1-LYRIC shRNA-B expression vector (desinaged as B) and control SAS cells (transfected with pLKO.1 vector, designated as CTL). Goal was to determine the effects of LYRIC knockdown on global SAS cells gene expression. Two-condition experiment, SAS cells transfected with pLKO.1-LYRIC shRNA-B expression vector (desinaged as B) v.s. control SAS cells (transfected with pLKO.1 vector, designated as CTL). Biological replicates: 4 control replicates, 4 transfected replicates.
Project description:Transcriptional profiling of SAS cells transfected with pLKO.1-LYRIC shRNA-B expression vector (desinaged as B) and control SAS cells (transfected with pLKO.1 vector, designated as CTL). Goal was to determine the effects of LYRIC knockdown on global SAS cells gene expression.
Project description:MicroRNAs (miRNAs) can act not only as tumor suppressor genes but also as oncogenes. Oncogenic miRNAs (oncomiRs) could therefore provide opportunities for the treatment of human malignancies. Here, we aimed to identify oncomiRs present in oral squamous cell carcinoma (OSCC) and addressed whether targeting these miRNAs might be useful in treatment for cancer. Functional screening for oncomiRs in a human OSCC cell line (GFP-SAS) was carried out using the miRCURY LNA microRNA Knockdown Library - Human version 12.0. We identified a locked nucleic acid (LNA)/DNA antisense oligonucleotide against miR-361-3p (LNA-miR-361-3p) which showed the largest degree of growth inhibition of GFP-SAS cells. Transfection with a synthetic mimic of mature miR-361-3p resulted in an approximately 20% increase in the growth of GFP-SAS cells. We identified odd-skipped related 2 (OSR2) as a miR-361-3p target gene. Transfection of GFP-SAS cells with LNA-miR-361-3p caused a significant increase in the expression levels of OSR2. Cotransfection of a OSR2 3'-UTR luciferase reporter plasmid and LNA-miR-361-3p into GFP-SAS cells produced higher levels of luciferase activity than in cells cotransfected with the LNA-nontarget. We assessed the effect of LNA-miR-361-3p on the in vivo growth of GFP-SAS cells. We found that LNA-miR-361-3p significantly reduced the size of s.c. xenografted GFP-SAS tumors, compared to the control group treated with LNA-NT. Finally, we observed that miR-361-3p is overexpressed in OSCC tissues. These results suggest that miR-361-3p supports the growth of human OSCC cells both in vitro and in vivo and that targeting miR-361-3p could be a useful therapeutic approach for patients with OSCC.