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Transgenic overexpression of the miR-200b/200a/429 cluster prevents mammary tumor development in MTB-TAN mice

ABSTRACT: Transgenic overexpression of the miR-200b/200a/429 cluster prevents mammary tumor development in MTB-TAN mice

PROVIDER: PRJNA1129144 | ENA |

REPOSITORIES: ENA

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Transgenic overexpression of the miR-200b/200a/429 cluster prevents mammary tumor development in MTB-TAN mice

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

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RNA sequencing of mammary glands from 55-day old control, MTB-200ba429, MTB-IGFIR, MTB-IGFIRba429 mice.

Project description:RNA was isolated from mammary glands from 55 day old control mice, mice overexpressing the miR-200b/200a/429 cluster in mammary epithelial cells (MTB-200ba429) mice overexpressing the IGF-IR transgene in mammary epithelial cells (MTB-IGFIR), and mice overexpressing both the miR-200b/200a/429 cluster and the IGF-IR transgene in mammary epithelial cells (MTB-IGFIRba429)

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The miR-200b/200a/429 cluster prevents metastasis and induces dormancy in murine claudin-low mammary tumor cells

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miR-200b/200a/429 cluster prevents metastasis and induces dormancy in murine claudin-low mammary tumor cells

Project description:miR-200b/200a/429 cluster prevents metastasis and induces dormancy in murine claudin-low mammary tumor cells

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The miR-200b/200a/429 cluster prevents metastasis and induces dormancy in murine claudin-low mammary tumor cells

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Searching for target genes of miR-429 in HCCLM3 cells

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.

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Timecourse of doxycycline induction in bitransgenic MTB/TAN, MTB/TOM, and MTB/TWNT1 mice or monotransgenic MTB control mice

Project description:Genome-wide expression data can provide important insights into normal and pathological cellular processes. However, the ability to use gene expression data to quantitatively assess the activation state of a given signaling pathway or transcriptional network in a sensitive and specific manner remains an important unmet goal. We now describe a computational algorithm, energy-paired scoring (EPS), that satisfies these criteria by predicting pathway activity using gene-gene interactions within a pathway signature in a manner analogous to the estimation of energy generated by two charged particles, as described by Coulomb’s law. We demonstrate the ability of EPS to: quantitatively assess pathway activation levels in vivo and in vitro; accurately estimate the extent of pathway inhibition achieved by gene knockdown; sensitively detect crosstalk between endogenous signaling pathways in vivo; and accurately identify compounds capable of inhibiting selected signaling pathways. Our findings indicate that EPS can accurately predict pathway activity over a wide dynamic range based upon gene expression data sets derived from multiple profiling platforms, as well as different species, tissues and cell types in both in vitro and in vivo contexts Four timepoints (0h, 24h, 48h and 96h) with 3 replicates per timepoint of doxycycline induction for MTB (Control), MTB/TAN, MTB/TOM and MTB/TWNT1

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