Project description:To clarify the effect of miRNAs, we carried out a gene expression microarray analysis of SW780 cells transfected with a miR-137 precursor or a negative control. We found that 1,326 probe sets (1,016 unique genes) were downregulated (>2-fold) by ectopic miR-137 expression, including the previously reported miR-137 target genes CDK6, CDC42 and AURKA. Moreover, Gene Ontology analysis revealed that genes related to the cell cycle were significantly enriched among the affected genes. SW780 cells were transfected with a Pre-miR-137 miRNA Precursor Molecule (Ambion) or Pre-miR miRNA Molecules Negative Control #1 (Ambion). Forty-eight hours after transfection, total RNA extraction was carried out, and gene expression signatures were analyzed.
Project description:We identified that miR-1 is silenced in association with CpG island hypermethylation in a colorectal cancer (CRC) cell line, HCT116. To determine whether miR-1 serves as a tumor suppressor in CRC, we transfected CRC cell lines with a miR-1 precursor molecule or a negative control, and carried then out a series of MTT assays. Forty-eight hours after transfection, we observed that ectopic expression of miR-1 moderately suppressed growth in all three cell lines. To further clarify the effect of the miRNA, we next performed gene expression microarray analysis in HCT116 cells transfected with a miR-1 precursor molecule or a negative control. We found that 2769 probe sets were downregulated (> 1.5-fold) by ectopic miR-1 expression, and gene ontology analysis revealed that “extracellular regions”, “membrane” and “response to wound healing” genes were significantly enriched among the downregulated genes. HCT116 cells were transfected with a Pre-miR-1 miRNA Precursor Molecule (Ambion) or Pre-miR miRNA Molecules Negative Control #1 (Ambion). Forty-eight hours after transfection, total RNA extraction were carried out, and gene expression signatures were analyzed.
Project description:To clarify the effect of miRNAs, we carried out a gene expression microarray analysis of SW780 cells transfected with a miR-137 precursor or a negative control. We found that 1,326 probe sets (1,016 unique genes) were downregulated (>2-fold) by ectopic miR-137 expression, including the previously reported miR-137 target genes CDK6, CDC42 and AURKA. Moreover, Gene Ontology analysis revealed that genes related to the cell cycle were significantly enriched among the affected genes.
Project description:We identified that miR-1 is silenced in association with CpG island hypermethylation in a colorectal cancer (CRC) cell line, HCT116. To determine whether miR-1 serves as a tumor suppressor in CRC, we transfected CRC cell lines with a miR-1 precursor molecule or a negative control, and carried then out a series of MTT assays. Forty-eight hours after transfection, we observed that ectopic expression of miR-1 moderately suppressed growth in all three cell lines. To further clarify the effect of the miRNA, we next performed gene expression microarray analysis in HCT116 cells transfected with a miR-1 precursor molecule or a negative control. We found that 2769 probe sets were downregulated (> 1.5-fold) by ectopic miR-1 expression, and gene ontology analysis revealed that “extracellular regions”, “membrane” and “response to wound healing” genes were significantly enriched among the downregulated genes.
Project description:To identify target genes of tumor suppressive microRNAs in human cancer, several cell lines (bladder cancer, prostate cancer, renal cell carcinoma, and head and neck squamous cell carcinoma) were subjected to Agilent whole genome microarrays. miR-517a, miR-218, miR-145, miR-1 and miR-874 function as tumor suppressors. Human cancer cell lines (BOY, T24, A498, PC3, DU145, FaDu, SAS, HSC3, IMC3) were transfected with miRNAs (miR-517a, miR-218, miR-145, miR-1, miR-874). The miRNA-transfected human cancer cell lines were compared to control cell lines.
Project description:We found frequent epigenetic silencing of microRNA-34b/c in human colorectal cancer. Introduction of miR-34b/c into a colorectal cancer cell line induced significant changes in gene expression profile. We also found overlap between the genes downregulated by miR-34b/c and those downregulated by DAC. Keywords: dose response A colorecal cancer cell line HCT116 was transfected with miR-34b or -c precursor or negative control. Also, HCT116 was treated with 5-aza-2'-deoxycytidine (DAC) or mock. Genes up- or downregulated by miR-34b/c and those by DAC was compared.
Project description:To identify target genes of cancer-related microRNAs in human cancer, several cell lines (bladder cancer, prostate cancer, renal cell carcinoma, esophageal squamous cell carcinoma, and head and neck squamous cell carcinoma) were subjected to Agilent whole genome microarrays. Human cancer cell lines (BOY, T24, A498, 786-O, caki-1, LNCap, PC3, TE2, T.Tn, FaDu, SAS, HSC3, and IMC-3) were transfected with miRNAs (miR-375, miR-145, miR-200a, miR-200b, miR-200c, miR-141, miR-429, miR-138, miR-218, miR-874, miR-31, miR-222, miR-1285, and miR-206) or siRNAs (si-FOXA1_1, si-FOXA1_3, and si-TAGLN2). The miRNA-transfected human cancer cell lines were compared to control cell lines.
Project description:Searching of target genes of miR-193b by transcriptome assay using 44K Whole Human Genome Microarray system (Agilent Technologies, Palo Alto, CA) resulted in finding of several candidate genes. To search of targets genes of miR-193b, we performed transcriptome analysis to compare expression profiles between human pancreatic cancer cells, MIA PaCa-2, transfected with precursor of miR-193b and those transfected with a negative control precursor.
Project description:To identify target genes of oncogenic or tumor suppressive microRNAs in human cancer, several cell lines (bladder cancer, prostate cancer, renal cell carcinoma. lung squamous cell carcinoma and head and neck squamous cell carcinoma) were subject to Agilent whole genome microarray. miR-183 and miR-96 function as oncogene. miR-1, miR-133a, miR-135a, miR-145 and miR-375 function as tumor suppressor The miRNA transfected human cancer cell lines (KK47, T24, A498, PC3, DU145, FaDu, SAS, PC10 and H157) were compared to control cell lines.