Project description:Investigation of whole genome gene expression level changes in miR-139-5p mimic-treated EC109 cells, compared to the scrambled negative controls. A four chip study using total RNA recovered from two separate cultures of miR-139-5p mimic-transfected EC109 cells and two separate cultures of scrambled negative control-transfected EC109 cells. Each chip measures the expression level of 44,049 genes from human esophageal cancer cell EC109 with three 60-mer probe pairs per gene.
Project description:Microarrays were used to characterize the global changes in miRNA expression in EC109 cells due to siRNA knockdown of long non-coding RNA MALAT1
Project description:Investigation of whole genome gene expression level changes in miR-139-5p mimic-treated EC109 cells, compared to the scrambled negative controls.
Project description:microarrays were used to characterize the global changes in gene expression in EC109 cells due to siRNA knockdown of long non-coding RNA MALAT1
Project description:Ezrin belongs to the ezrin¨Cradixin¨Cmoesin (ERM) family proteins, which cross-link actin cytoskeleton and plasma membrane, and is actively involved in regulating the growth and metastatic capacity of cancer cells. Esophageal squamous cell carcinoma (ESCC) is one of the most fatal malignancies in the world and the expression of ezrin in ESCC has been described only recently, but its roles and mechanism still remained unclear. we have used the pSUPER RNAi system to stably suppress the expression of the ezrin gene in EC109, an esophageal squamous carcinoma cell line, and then cDNA microarray was performed to explore some changed genes with ezrin silence. Keywords: Gene expression after RNAi
Project description:We constructed EC109 cells transfected by lncRPL34-AS1 plasmid and scramble pcDNA to select differentially expressed genes and transcripts
Project description:Ezrin belongs to the ezrin¨Cradixin¨Cmoesin (ERM) family proteins, which cross-link actin cytoskeleton and plasma membrane, and is actively involved in regulating the growth and metastatic capacity of cancer cells. Esophageal squamous cell carcinoma (ESCC) is one of the most fatal malignancies in the world and the expression of ezrin in ESCC has been described only recently, but its roles and mechanism still remained unclear. we have used the pSUPER RNAi system to stably suppress the expression of the ezrin gene in EC109, an esophageal squamous carcinoma cell line, and then cDNA microarray was performed to explore some changed genes with ezrin silence. Experiment Overall Design: he mammalian expression vector, pSUPER.neo.circular (OligoEngine), was used for expression of siRNA in EC109 cells. Briefly, two primer pairs were synthesized, one pair encoding nucleotides 274¨C292 (TCCACTATGTGGATAATAA) followed by a 9 base ¡®¡®loop¡¯¡¯ (TTCAAGAGA) and the inverted repeat (PSE1), and the second encoding nucleotides 265¨C283 (ACTTTGGCCTCCACTATGT) again followed by the loop and inverted repeat (PSE2). And pSUPER.neo vector of nonspecific siRNA was taken as negative control (PSC). The primer pairs were annealed and inserted into the BglII and HindIII sites of pSUPER.neo and transformed into JM109 competent cells (Promega). Positive clones were verified and transfected into EC109 cells using FuGENE 6 transfection reagent (Roche) according to the manufacturer¡¯s instructions. G418 (400 ¦Ãg/ml, Calbiochem) was added into the culture medium after 24 h. Stable G418-resistant clones were obtained in 7¨C9 days. The expanded cells were then used for subsequent studies.
Project description:Expression data from different expressed genes (DEGs) in human esophageal squamous cell carcinoma (ESCC) EC109 cells transfected with empty lentiviral vector (Lv-NC) or lentiviral vector carrying carrying KDM5C specific shRNA (Lv-shKDM5C) Lysine demethylase 5C (KDM5C), a member of lncRNAs, has tumor-suppressor properties and is downregulated in the majority of malignancies. KDM5C was found to suppress some sorts of tumors through regulating epithelial mesenchymal transformation,inducing cell cycle arrest,triggering apoptosis and so on. We used microarrays to investigate the possible regulatory mechanism of KDM5C in ESCC cell line.