Expression signature in a human colorectal cancer cell lines, HCT116 and RKO, transfected with miR-101. Homo sapiens

Understanding of molecular system how tumor-suppressor p53 selectively activates and/or completes appropriate tumor-suppressor pathway in response to various stresses is still one of the most important issues to be clarified. We analyzed a molecular mechanism for the completion of p53-dependent ribosome stress responsible pathway by miR-101. To this end, expression microarray analyses were conducted in the presence or absence of miR-101. We found that miR-101 induces the activation of p53-dependent G2 phase cell cycle arrest through the increased phosphorylation of ATM, leading to the p53-depdent apoptosis. Overall design: HCT116 or RKO cells were transfected with a Pre-miR-101 miRNA Precursor Molecule (Ambion) or Pre-miR miRNA Molecules Negative Control #2 (Ambion) at a final concentration of 5 nM. After incubtion for 3 days, total RNAs were extracted and gene expression signatures were determined. Three independent experiments were performed for each transfection.