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Gene expression after treatment with anti-miR-191 or control

ABSTRACT: The goal of this experiment was to identify possible genes affected directly or indirectly by anti-miR-191. Hepatocellular carcinoma (HCC) is a fatal disease with currently very limited beneficial therapies. MicroRNAs (miRs), which are considered to be master regulators of gene expression, have significant influence on cellular pathways and phenotype, and are de-regulated in HCC, and hence are thought to be of great therapeutic potential as novel targets. We identified hsa-miR-191 as a potential target for HCC therapy. Inhibition of this miR causes decreased cell proliferation and induction of apoptosis in vitro as well as a significant reduction of tumor mass in vivo in an orthotopic liver xenograft model. This miR was also found to be up-regulated by a dioxin, a known liver carcinogen, and was found to be a key regulator of cancer related pathways.

ORGANISM(S): Homo sapiens

PROVIDER: GSE22790 | GEO | 2011/07/01

SECONDARY ACCESSION(S): PRJNA129147

REPOSITORIES: GEO

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Project description:This study represents the first attempt to perform a profiling analysis of the intergenerational differences in the microRNAs (miRNAs) of melanocytic neoplasms in young adult and older adult groups. Our comparative miRNA profiling provides a novel characterization of the miRnomes of melanocytic neoplasms and melanomas of different age groups and identifies a set of potential diagnostic and potential clinico-pathologic biomarkers that may serve as targets for development of novel miR-based modalities in cancer diagnosis and treatment. An exploratory miRNA analysis of 666 miRs was conducted on formalin fixed and paraffin embedded tissues from 10 adults and 10 young adults including conventional melanoma and melanocytic neoplasms of uncertain biological significance. Age-matched benign melanocytic nevi were used as controls. The comparative profiling was intentionally performed at two extremes of age, i.e., less than 30 years (Mel 30) and greater than 60 years (Mel 60). Primary melanoma in patients greater than 60 years old was characterized by the increased expression of miRs regulating TLR-MyD88-NF-kappaB pathway (hsa-miR -199a), RAS/RAB22A pathway (hsa-miR-204); growth differentiation and migration (hsa-miR337), epithelial mesenchymal transition EMT (let-7b, hsa-miR-10b/10bSTAR(*)), invasion and metastasis (hsa-miR-10b/10bSTAR(*), hsa-miR-30a/e*, hsa-miR-29c*; cellular matrix components (hsa-miR-29c*); invasion-cytokinesis (hsa-miR 99b*) compared to melanoma of younger patients. miR 211 was dramatically downregulated in primary melanoma compared to nevi controls, decreased with increasing age and was among the miRs linked to metastatic processes and potentially targeting the inflammatory receptor CCR10; Primary melanoma in young adult patients was characterized by the increased expression of hsa-miR-449a and decreased expression of hsa-miR146b, hsa-miR 214*. Among the miRs expressed at higher levels in control nevi, compared to adult or young adult melanoma, was hsa-miR 574-3p. Only 2 miRs distinguished adult from young adult-pediatric nevi, hsa-miR374a* and has-miR-566. MiR 30a* appeared to be a strong marker of differentiation in clinical stages I-II adult and pediatric melanoma, and could predict classification of melanoma tissue in the two age groups. Furthermore, lymph node status in the two age groups was characterized by the statistically significant expression of hsa-miR-30a* and hsa-miR-204 (F-test, p-value <0.001).

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Gene expression after treatment with anti-miR-191 or control

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