Differential expression of miRNA in stage-specific prostate cancer
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ABSTRACT:
PROVIDER: PRJNA488806 | ENA |
REPOSITORIES: ENA
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Project description:Dysregulation of microRNAs (miRNAs) can majorly contribute to prostate cancer tumor development, progression, and are differentially expressed in normal and cancer tissues. Glass-based chip assay was designed for prostate cancer cell lines; from early disease stage to advance and to castration resistance prostate cancer (CRPC). We have used glass based chip microarray assay (miRNA-microarray); and our attempt identified that the expression of miR-301 was upregulated at early stage and miR- 146/146b showed increased in expression during the advanced stage of prostate cancer. While the expression of miR-205 and miR-221 was consistently downregulated across all the disease stage; from early to advanced and also during the CRPC stage. Also, we have identified some disease-specific/signature miRNAs for e.g. miR-204 which was differentially expressed only during early stage of prostate cancer and miR-520 was during CRPC stage.
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Project description:MicroRNAs (miRNAs, miRs) modulate a multitude of cellular events. Here, we identify functional miRNA-protein networks that regulate human monocyte-derived dendritic cell (MDDC) differentiation. MiRNA profiling revealed stage-specific differential expression of 20 miRNAs during days 1, 3 and 5 of MDDC differentiation. To identify and prioritize miRNA-protein networks for functional validation, we developed a target ranking algorithm that incorporates many features of miRNA regulatory networks. This system prioritized miR-21, miR-34a, and their cognate targets WNT1 and JAG1 for functional validation. Inhibition of both miR-21 and miR-34a stalled MDDC differentiation, as quantified by DC-SIGN/CD14 expression ratios, showing cooperative involvement of these miRNAs in MDDC differentiation. We confirmed that the 3’ UTRs of WNT1 and JAG1 were functional targets of these miRNAs and provide evidence that these targets were translationally suppressed. Significantly, exogenously added Wnt-1 and Jagged-1 also stalled MDDC differentiation, suggesting that miRNA mediated inhibition of endogenous WNT1 and JAG1 expression was important for proper MDDC differentiation. Finally, inhibition of miR-21 and miR-34a, or addition of Wnt-1 and Jagged-1 led to a decrease in endocytic capacity, a key function of immature DCs. Thus, our novel approach identified and validated some miRNA-protein networks involved in phenotypic and functional MDDC differentiation.
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Project description:MicroRNAs (miRNAs, miRs) modulate a multitude of cellular events. Here, we identify functional miRNA-protein networks that regulate human monocyte-derived dendritic cell (MDDC) differentiation. MiRNA profiling revealed stage-specific differential expression of 20 miRNAs during days 1, 3 and 5 of MDDC differentiation. To identify and prioritize miRNA-protein networks for functional validation, we developed a target ranking algorithm that incorporates many features of miRNA regulatory networks. This system prioritized miR-21, miR-34a, and their cognate targets WNT1 and JAG1 for functional validation. Inhibition of both miR-21 and miR-34a stalled MDDC differentiation, as quantified by DC-SIGN/CD14 expression ratios, showing cooperative involvement of these miRNAs in MDDC differentiation. We confirmed that the 3â UTRs of WNT1 and JAG1 were functional targets of these miRNAs and provide evidence that these targets were translationally suppressed. Significantly, exogenously added Wnt-1 and Jagged-1 also stalled MDDC differentiation, suggesting that miRNA mediated inhibition of endogenous WNT1 and JAG1 expression was important for proper MDDC differentiation. Finally, inhibition of miR-21 and miR-34a, or addition of Wnt-1 and Jagged-1 led to a decrease in endocytic capacity, a key function of immature DCs. Thus, our novel approach identified and validated some miRNA-protein networks involved in phenotypic and functional MDDC differentiation. monocytes were cultured with GM-CSF and IL-4 for the indicated days (0,1, 3, and 5). Each timepoint was repeated in 3 independent donors (donor 1 , 2, and 3).
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