Project description:This study aimed to investigate the metastasis-related prognostic gene signature in lung cancer. We started from the genowide miRNAs profiling of 16 lung adenocarcinoma cells. We identified that miR-10a* is an invasion-based prognostic gene in lung adenocarcinoma. Besides, we used expression beadsarray to identify the global gene alterations in HOP-62 cells after ectopic introducing miR-10a* and ectopic expressing HDAC5 genes.
Project description:This study aimed to investigate the metastasis-related prognostic gene signature in lung cancer. We started from the genowide miRNAs profiling of 16 lung adenocarcinoma cells. We identified that miR-10a* is an invasion-based prognostic gene in lung adenocarcinoma. Besides, we used expression beadsarray to identify the global gene alterations in HOP-62 cells after ectopic introducing miR-10a* and ectopic expressing HDAC5 genes.
Project description:MicroRNAs (miRNAs) are small RNAs that function as post-transcriptional regulators of gene expression. miRNAs affect a variety of signaling pathways and impaired miRNA regulation may contribute to the development of cancer and other diseases. We show that miRNA miR-10a interacts with the 5' untranslated region of mRNAs encoding ribosomal proteins and enhances their translation. miR-10a alleviates translational repression of the ribosomal protein mRNAs during amino acid starvation and is required for their stress-mediated activation following anisomycin treatment. miR-10a binds immediately downstream of the regulatory 5' TOP motif and the 5´TOP is necessary for miR-10a translational enhancement. The results indicate that miR-10a may positively control global protein synthesis via stimulation of ribosomal protein mRNA translation and that the 5' TOP regulatory complex and miR-10a are functionally interconnected.
Project description:MiR-10a inhibits colon cancer invasion and metastasis. To search the candidate target genes of miR-10a, SW480 cells were transfected with miR-10a blockage to suppress miR-10a activity and the differentially expressed genes were detected by cDNA microarray analysis. Some of the up-regulated genes may be candidate target genes of miR-10a.
Project description:miR-10a has been shown to regulate proliferation and invasiveness of cancer cells and inflammatory responses of endothelial cells. The function of miR-10a in the skin has not been studied before. Here we examined miR-10a expression, regulation and functions in keratinocytes (KCs) in association with atopic dermatitis (AD).
Project description:MicroRNA (miRNA) is a family of small regulatory RNA that post-transcriptionally regulates many biological functions including growth and development. Chicken miR-143 and miR-10a are expressed in both the embryonic and post-hatch chick in a spatio-temporal manner. In order to study the functions of these miRNAs, loss of function and microarray approaches were employed. Spleen cells were isolated from embryonic day 18 chickens and immediately transfected with either a synthetic miR-143 inhibitor or a synthetic miR-10a inhibitor or a negative control oligo-nucleotide (Dharmacon). Cultures were maintained for 48 hrs and microarray analysis was performed using the Arizona Gallus gallus 20.7K long oligoarray (GPL6049). Differentially expressed genes were identified for each miRNA by comparing the miRNA knock-down group to the negative control group. The differentially expressed genes were functionally categorized using the DAVID Functional Annotation Tool (http://david.abcc.ncifcrf.gov/). The 3’-UTR of the up-regulated genes (de-repressed after the miRNAs knock-down) were scanned for potential miR-143 or miR-10a binding sites using the miRanda algorithm version 3.1 (http://www.microrna.org/microrna). In addition, the Chicken (Gallus gallus) Unigene database (NCBI) was also used to predict potential targets of these miRNAs. A set of predicted targets for both miRNAs was selected and validated by dual luciferase reporter gene assay. Overall, many of the identified targets for miR-143 are associated with cell proliferation, tumerigenesis and apoptosis. Many of potential targets for miR-10a are associated with immune response.
Project description:This study investigates the miR-10a-mediated transcriptome in human aortic endothelial cells (HAECs). The EC transcriptome was profiled in miR-10a knockdown HAECs. Specifically, small amounts of EC RNA were isolated from control cells and miR-10 knockdown cells expressing miRNA inhibitor control (Dharmacon) and miR-10a inhibitors (Dharmacon), respectively . Eight 2-channel assays comparing knockdown to control were performed using the Agilent Whole Human Genome Microarray 4x44K [G4112F].
Project description:In multiple myeloma (MM), abnormal plasma cells interact with bone marrow (BM) stromal cells and vascular cells among others. Bone marrow stromal cells (BMSCs) interact with MM cells in the bone marrow (BM), and also create a permissive microenvironment for MM cell growth and survival. Recent evidence indicated that extracellular vesicles (EVs)-mediated MM cell-BMSC communication plays an important role in the MM microenvironment. In this study, we investigated the biological property of the EVs and EV-miRNAs derived from BMSCs, aiming to establish the emerging strategies to target MM microenvironment to prevent tumor growth and spread. We found that the MM-BMSC-EVs enhanced the cell proliferation of RPMI8226. The EV-miRNA expression was different between MM-BMSCs and Normal-BMSCs, and some miRNAs, including miR-10a, were significantly up-regulated in the MM-BMSC-EVs. We then visualized with an in vitro model the uptake of Cy3-labeled miR-10a into RPMI8226 via EVs. To identify the function of miR-10a in MM cells, miR-10a mimic was transfected into RPMI8226 cells.
Project description:MicroRNA (miRNA) is a family of small regulatory RNA that post-transcriptionally regulates many biological functions including growth and development. Chicken miR-143 and miR-10a are expressed in both the embryonic and post-hatch chick in a spatio-temporal manner. In order to study the functions of these miRNAs, loss of function and microarray approaches were employed. Spleen cells were isolated from embryonic day 18 chickens and immediately transfected with either a synthetic miR-143 inhibitor or a synthetic miR-10a inhibitor or a negative control oligo-nucleotide (Dharmacon). Cultures were maintained for 48 hrs and microarray analysis was performed using the Arizona Gallus gallus 20.7K long oligoarray (GPL6049). Differentially expressed genes were identified for each miRNA by comparing the miRNA knock-down group to the negative control group. The differentially expressed genes were functionally categorized using the DAVID Functional Annotation Tool (http://david.abcc.ncifcrf.gov/). The 3â-UTR of the up-regulated genes (de-repressed after the miRNAs knock-down) were scanned for potential miR-143 or miR-10a binding sites using the miRanda algorithm version 3.1 (http://www.microrna.org/microrna). In addition, the Chicken (Gallus gallus) Unigene database (NCBI) was also used to predict potential targets of these miRNAs. A set of predicted targets for both miRNAs was selected and validated by dual luciferase reporter gene assay. Overall, many of the identified targets for miR-143 are associated with cell proliferation, tumerigenesis and apoptosis. Many of potential targets for miR-10a are associated with immune response. A reference designed microarray was performed in which samples (Cy3) were co-hybridized with the reference RNA pool (Cy5) on the array. The microarray data set was processed using within- and across-array loess normalization method in JMP Genomics 3.0, SAS (Cary, NC). Data quality was evaluated using the MA plots process and the correlation and grouped scatter plots procedure (JMP Genomics 3.0). Differentially expressed genes were identified using ANOVA process on JMP Genomics 3.0 with fixed effect of treatments and random effect of arrays.
Project description:A variety of CD4+Foxp3+ Treg cell types have been described previously, indicating molecular heterogeneity within the Foxp3+ pool of CD4+ T cells. However, the factors that shape the transcriptomic identities of different Foxp3+ Treg cells are poorly understood. To identify the molecular pathways involved, we isolated CD4+Foxp3gfp+ cells from Th1-rich or Th2-rich environments following chronic Leishmania major or Schistosoma mansoni infection, respectively. Whole genome expression profiling and next generation small RNA sequencing revealed significantly different mRNA and miRNA profiles. In-silico analyses identified miR-10a and miR-182 as ‘regulatory miRNA hubs’ in CD4+Foxp3+ cells in Th1 and Th2-environments, respectively. Using in vitro and in vivo systems we identified that IL-12/IFNg down-regulated miR-10a and its putative transcription factor, Creb. Importantly, we demonstrated that miR-10a controls a suite of genes that regulate IFNg production in Th1-Treg cells. Also, Treg cells treated with IL-4 increased miR-182 and its putative transcription factor, cMaf. Up-regulation of miR-182 mitigated IL-2 secretion, in part through repression of IL2-promoting genes, including Bach2 and Cd2ap. This study indicates that CD4+Foxp3+ cells are influenced by their environment, and that Th1 or Th2 environments promote distinct miRNA pathways, preserving Treg stability and suppressor function.