Project description:miRNAs are an class of small noncoding RNAs and about 21-25 nucleotides in length. miRNAs inhibit the translation or induce mRNA degradation by binding to the 3’ UTR of target mRNAs and have been identified as the tumor promoters or suppressors regulating the progression of cancers. miR-429, which is a member of an evolutionarily conserved family of miRNAs that includes miR-200b, miR-200a, miR-200c and miR-141, is expressed in various epithelial tissues. Our goal is to search the possible target genes of miR-429 in human liver cancer cell line HCCLM3. We analyzed possible target genes of miR-429 by identifying the shared genes among the down-regulated genes in epithelial cell adhesion molecule (EpCAM) negative HCCLM3 cells which treated with miR-429 mimics and the up-regulated genes in EpCAM positive HCCLM3 cells which treated with Antagomir-429.
Project description:Transcriptome profile of optic cups from RhoP23H/+ mice following AAV-mediated subretinal delivery of pre-miR-429 or GFP (control vector) to study the molecular changes underlying the neuroprotective effect of miR-429 overexpression in an Inherited Retinal Disease (IRD) model.
Project description:We have previously shown that transgenic overexpression of the miR-200b/200a/429 cluster prevents mammary tumor development in MTB-IGFIR mice. In this study we evaluated whether the miR-200b/200a/429 cluster could also prevent mammary tumor development from a different oncogene, namely Neu/Erbb2. We found that transgenic overexpression of Neu/Erbb2 in MTB-TAN mice induce rapid mammary tumor development and co-overexpression of the miR-200b/200a/429 cluster with Neu/Erbb2 completely prevent mammary epithelial transformation and tumor development