Similar Datasets
Project description:RNA-seq on miRNA induced mouse keratinocytes. miR-200b cluster and miR-205.
| PRJNA542900 | ENA
Project description:BackgroundY-box binding protein 1 (YB1 or YBX1) plays a critical role in tumorigenesis and cancer progression. However, whether YB1 affects malignant transformation by modulating non-coding RNAs remains largely unknown. This study aimed to investigate the relationship between YB1 and microRNAs and reveal the underlying mechanism by which YB1 impacts on tumor malignancy via miRNAs-mediated regulatory network.MethodsThe biological functions of YB1 in hepatocellular carcinoma (HCC) cells were investigated by cell proliferation, wound healing, and transwell invasion assays. The miRNAs dysregulated by YB1 were screened by microarray analysis in HCC cell lines. The regulation of YB1 on miR-205 and miR-200b was determined by quantitative real-time PCR, dual-luciferase reporter assay, RNA immunoprecipitation, and pull-down assay. The relationships of YB1, DGCR8, Dicer, TUT4, and TUT1 were identified by pull-down and coimmunoprecipitation experiments. The cellular co-localization of YB1, DGCR8, and Dicer were detected by immunofluorescent staining. The in vivo effect of YB1 on tumor metastasis was determined by injecting MHCC97H cells transduced with YB1 shRNA or shControl via the tail vein in nude BALB/c mice. The expression levels of epithelial to mesenchymal transition markers were detected by immunoblotting and immunohistochemistry assays.ResultsYB1 promoted HCC cell migration and tumor metastasis by regulating miR-205/200b-ZEB1 axis partially in a Snail-independent manner. YB1 suppressed miR-205 and miR-200b maturation by interacting with the microprocessors DGCR8 and Dicer as well as TUT4 and TUT1 via the conserved cold shock domain. Subsequently, the downregulation of miR-205 and miR-200b enhanced ZEB1 expression, thus leading to increased cell migration and invasion. Furthermore, statistical analyses on gene expression data from HCC and normal liver tissues showed that YB1 expression was positively associated with ZEB1 expression and remarkably correlated with clinical prognosis.ConclusionThis study reveals a previously undescribed mechanism by which YB1 promotes cancer progression by regulating the miR-205/200b-ZEB1 axis in HCC cells. Furthermore, these results highlight that YB1 may play biological functions via miRNAs-mediated gene regulation, and it can serve as a potential therapeutic target in human cancers.
| S-EPMC8286141 | biostudies-literature
Project description:A screen of microRNA (miRNA) expression following differentiation in human foreskin keratinocytes (HFKs) identified changes in several miRNAs, including miR-24 and miR-205. We investigated how expression of Human Papilloma Virus Type-16 (HPV16) onco-proteins E6 and E7 affected expression of miR-24 and miR-205 during proliferation and differentiation of HFKs. We show that the induction of both miR-24 and miR-205 observed during differentiation of HFKs is lost in HFKs expressing E6 and E7. We demonstrate that the effect on miR-205 is due to E7 activity, as miR-205 expression is dependent on pRb expression. Finally, we provide evidence that miR-24 effects in the cell may be due to targeting of cyclin dependent kinase inhibitor p27. In summary, these results indicate that expression of both miR-24 and miR-205 are impacted by E6 and/or E7 expression, which may be one mechanism by which HPV onco-proteins can disrupt the balance between proliferation and differentiation in keratinocytes.
| S-EPMC3865362 | biostudies-literature
Project description:For androgen-independent prostate cancer (AIPC), the current treatment is limited and the prognosis is poor. We previously found miR-200b could inhibit androgen independent proliferation ability of prostate cancer cells, but the mechanism is unclear. MiRNAs plays their role by blocking translation through base-pairing with complementary mRNA and by promoting degradation of target mRNA. Unraveling the miRNA translational silencing network remains a challenge in part because a single miRNA can inhibit multiple mRNA targets and because a single mRNA can be regulated by several distinct miRNAs that act cooperatively. However, proteomics methods provide us useful tools to unravel the target genes network. This study identified the target genes of miR-200b in AIPC. It helps us to understand the mechanism of AIPC and applies several new candidate targets of AIPC treatment.
2020-08-05 | PXD006350 | Pride
Project description:We used miRNA expression arrays and integrated analysis to study mucoepidermoid carcinomas (MEC) to identify potential drivers involved with its pathogenesis. Normal salivary glands were used as controls.
2022-03-03 | GSE169692 | GEO
Project description:Microarray‐based techniques are being used to obtain miRNA and gene expression signatures associated with different samples. In order to deepen our understanding of BRCA1-associated tumorigenesis, we integrated data from microarray experiments to obtain significant miRNA-mRNA relationships associated with the presence of the BRCA1 gene. We obtained significant miRNA-gene-pathway relationships underlying the array signatures. Furthermore, we have demonstrated that miR-146a, miR-99b and miR-205, induced in HCC1937 BRCA1-expressing cells, commonly regulate the TRAF2 gene, a key regulator of NF-κB and MAPK pathways. In addition, re-expression of miR-146a, miR-99b or miR-205 in HCC1937 BRCA1-null cells was sufficient to modulate NF-κB activity. Thus, integration between miRNA-mRNA expression data allowed us to define genes and pathways controlled by miRNAs induced in the context of BRCA1 expression.
2011-12-24 | GSE30763 | GEO
Project description:Microarray‐based techniques are being used to obtain miRNA and gene expression signatures associated with different samples. In order to deepen our understanding of BRCA1-associated tumorigenesis, we integrated data from microarray experiments to obtain significant miRNA-mRNA relationships associated with the presence of the BRCA1 gene. We obtained significant miRNA-gene-pathway relationships underlying the array signatures. Furthermore, we have demonstrated that miR-146a, miR-99b and miR-205, induced in HCC1937 BRCA1-expressing cells, commonly regulate the TRAF2 gene, a key regulator of NF-κB and MAPK pathways. In addition, re-expression of miR-146a, miR-99b or miR-205 in HCC1937 BRCA1-null cells was sufficient to modulate NF-κB activity. Thus, integration between miRNA-mRNA expression data allowed us to define genes and pathways controlled by miRNAs induced in the context of BRCA1 expression. Comparison of miRNA expression profiles between two isogenic cell lines differing in BRCA1 gene expression status. Single-color experiments in a pairwise comparison design with three technical replicates per cell line.
| S-ECPF-GEOD-30763 | biostudies-other
Project description:Micro RNAs (miRNAs) miR-130a, miR-203 and miR-205 are jointly downregulated in prostate cancer and act as repressors of AR-signaling. MiRNAs are small non-coding RNAs that regulate the expression of specific mRNA targets mainly by translational repression, mRNA deadenylation or cleavage. Reconstitution of these lost miRNAs in the LNCaP PCa cell line cause morphology changes, growth arrest, and apoptosis, increasing when the miRNAs were co-expressed. This series identifies direct targets of miR-130a, miR-203, and miR-205 by AGO2-RNA co-immunoprecipitation as described by (Beitzinger et al. 2007) upon miRNA reconstitution in LNCaP cells and analyzing AGO2-bound mRNAs using Affymetrix Genechips. Relative levels of AGO2 bound versus total RNA expression were compared between miRNA reconstituted and miR-scr transfected samples.
2012-03-08 | GSE22979 | GEO
Project description:The miR-200 family consists of five members expressed as two clusters: miR-200c/141 cluster and miR-200b/200a/429 cluster. In the mammary gland, miR-200s maintain epithelial identity by decreasing the expression of mesenchymal markers leading to high expression of epithelial markers. While the loss of miR-200s is associated with breast cancer growth and metastasis the impact of miR-200 expression on mammary tumor initiation has not been investigated. Using mammary specific expression of the miR-200b/200a/429 cluster in transgenic mice, we found that elevated expression miR-200s could almost completely prevent mammary tumor development. Only 1 of 16 MTB-IGFIRba429 transgenic mice (expressing both the IGF-IR and miR-200b/200a/429 transgenes) developed a mammary tumor while 100% of MTB-IGFIR transgenic mice (expressing only the IGF-IR transgene) developed mammary tumors. RNA sequencing, qRT-PCR, and immunohistochemistry of mammary tissue from 55-day old mice found Spp1, Saa1, and Saa2 to be elevated in mammary tumors and inhibited by miR-200b/200a/429 overexpression. This study suggests that miR-200s could be used as a preventative strategy to protect women from developing breast cancer. One concern with this approach is the potential negative impact miR-200 overexpression may have on mammary function. However, transgenic overexpression of miR-200s, on their own, did not significantly impact mammary ductal development indicating the miR-200 overexpression should not significantly impact mammary function. Thus, this study provides the initial foundation for using miR-200s for breast cancer prevention and additional studies should be performed to identify strategies for increasing mammary miR-200 expression and determine whether miR-200s can prevent mammary tumor initiation by other genetic alterations.
| S-EPMC8473771 | biostudies-literature
Project description:BackgroundRecent studies have extensively investigated the role of miRNAs in colorectal cancer (CRC), and several associations have been reported. In addition, single nucleotide polymorphisms (SNPs) in promoter regions of miRNAs have been shown to affect miRNA expression. Therefore, we aimed to analyze the effect of miRNA polymorphisms on CRC susceptibility.MethodsWe conducted association studies on the relationships between the miRNA polymorphisms miR-130bT > C rs373001, miR-200bT > C rs7549819, and miR-495A > C rs2281611 and CRC with 472 CRC patients and 399 control subjects in Korea.ResultsMultivariate logistic regressions of the CRC subgroups showed that the miR-495CC genotype associated with rectal cancer (AA+AC vs. CC; adjusted odds ratio (AOR) for CC, 1.592; 95% confidence interval (CI), 1.071-2.368; P = 0.022). The gene-environment combinatorial analysis showed that the combination of miR-495A > C and low plasma folate contributed to an increased risk of rectal cancer (AA+AC vs. CC; AOR for CC, 3.829; 95% CI, 1.577-9.300; P = 0.003). In the survival analysis, miR-200bT > C associated with CRC patient mortality (TT vs TC + CC; adjusted hazard ratio for TC + CC, 0.592; 95% CI, 0.373-0.940; P = 0.026).ConclusionIn this study, we found that miR-200b and miR-495 polymorphisms are involved in CRC susceptibility and prognosis.
| S-EPMC6532172 | biostudies-literature