MiR-196b-5p and miR-107 expression differentiates ocular sebaceous carcinoma from squamous cell carcinoma of the comjunctiva
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PROVIDER: PRJNA831876 | ENA |
REPOSITORIES: ENA
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Project description:Ocular Sebaceous Carcinoma (OSC) is a rare malignant tumor for which initial clinical and pathological diagnosis is often incorrect. OSC can mimic Squamous Cell Carcinoma of the Conjunctiva (SCCC). Aim of this study was to find microRNA biomarkers to distinguish OSC and SCCC from normal tissue and from each other. Clinical OSC and SCCC case files and corresponding histopathological slides were collected and reviewed. Microdissected formalin-fixed paraffin-embedded tumor and control tissue were sub-jected to semi-high throughput microRNA profiling. MicroRNA expression distinguishes OSC and SCCC from corresponding control tissues. Selected differentially expressed miRNAs were validated using single RT-PCR assays. No prognostic miRNAs could be identified that reliable predict SCCC metastasis or OSC recurrence. A com-parison between OSC (n=14) and SCCC (n=18) revealed 38 differentially expressed microRNAs (p<0.05). Differentially expressed miRNAs were selected for validation in the discovery cohort and an independent validation cohort (OSC, n=11; SCCC, n=12). At least two miRNAs miR-196b-5p (p ≤ 0.05) and miR-107 (p ≤ 0.001) displayed a statistically significant differential expression between OSC and SCCC with miR-196b-5p upregulated in SCCC and miR-107 up-regulated in OSC. In the validation cohort microRNA miR-493-3p also showed significant up-regulation in SCCC when compared to OSC (p ≤ 0.05). ROC analyses indicated that the com-bined miR-196b-5p and miR-107 expression levels predicted OSC with 90.0% sensitivity and 83.3% specificity. In conclusion, combined testing of miR-196b-5p and miR-107, can be of additional use in routine diagnostics to discriminate OSC from SCCC.
2022-04-26 | GSE201490 | GEO
Project description:Sebaceous gland carcinoma is the frequent malignant tumor of the eyelid. However, there is limited understanding of how altered gene expression of sebaceous gland carcinoma of the eyelid related to the pathogenesis. In this study, to identify genes involved in sebaceous gland carcinoma of the eyelid, global-scale gene expression analysis was carried out using a GeneChip® system.
2019-01-25 | GSE125582 | GEO
Project description:To screen the related miRNAs in the occurence and development of sebaceous gland carcinoma(SGC) of the eyelid , we have employed Human Agilient microarray expression profiling as a discovery platform to identify differentially expressed miRNAs for SGC and TP53 mtation related miRNAs. Human formalin-fixed paraffin-embedded (FFPE) SGC tissues and para-carcinoma sebaceous gland(SG) FFPE samples from SGC patients were screened using microarray assay. Human FFPE SGC tissues containing TP53 mutation and human FFPE SGC tissues without TP53 mutation were screened using microarray. The overlap of two sets of microarray differentially upregulated miRNAs were selected as our research object.
2021-09-01 | GSE182876 | GEO
Project description: Not available
| S-EPMC9102373 | biostudies-literature
Project description:MicroRNA silencing by promoter hypermethylation may represent a mechanism by which lung cancer develops and progresses, but the microRNAs involved during malignant transformation are unknown. We previously established a model of pre-malignant lung cancer wherein we treated human bronchial epithelial cells (HBEC) with low doses of tobacco carcinogens. Here, we demonstrate that next-generation sequencing of carcinogen-transformed HBECs treated with the demethylating agent 5-aza-2'deoxycytidine revealed miR-196b and miR-34c-5p to be epigenetic targets. Bisulfite sequencing confirmed dense promoter hypermethylation indicative of silencing in multiple malignant cell lines and primary tumors. Chromatin immunoprecipitation studies further demonstrated an enrichment in repressive histone marks on the miR-196b promoter during HBEC transformation. Restoration of miR-196b expression by transfecting transformed HBECs with specific mimics led to cell cycle arrest mediated in part through transcriptional regulation of the FOS oncogene, and miR-196b re-expression also significantly reduced the growth of tumor xenografts. Luciferase assays demonstrated that forced expression of miR-196b inhibited the FOS promoter and AP-1 reporter activity. Finally, a case-control study revealed that methylation of miR-196b in sputum was strongly associated with lung cancer (OR = 4.7, p<0.001). Collectively, these studies highlight miR-196b as a tumor suppressor whose silencing early in lung carcinogenesis may provide a selective growth advantage to pre-malignant cells. Targeted delivery of miR-196b could therefore serve as a preventive or therapeutic strategy for the management of lung cancer. HBEC2MBT and H1975 were transiently transfected with a miR-196b mimic and subjected to array-based genome-wide gene expression profiling 48 hours post transfection.
2016-09-09 | GSE79987 | GEO
Project description:MicroRNA silencing by promoter hypermethylation may represent a mechanism by which lung cancer develops and progresses, but the microRNAs involved during malignant transformation are unknown. We previously established a model of pre-malignant lung cancer wherein we treated human bronchial epithelial cells (HBEC) with low doses of tobacco carcinogens. Here, we demonstrate that next-generation sequencing of carcinogen-transformed HBECs treated with the demethylating agent 5-aza-2'deoxycytidine revealed miR-196b and miR-34c-5p to be epigenetic targets. Bisulfite sequencing confirmed dense promoter hypermethylation indicative of silencing in multiple malignant cell lines and primary tumors. Chromatin immunoprecipitation studies further demonstrated an enrichment in repressive histone marks on the miR-196b promoter during HBEC transformation. Restoration of miR-196b expression by transfecting transformed HBECs with specific mimics led to cell cycle arrest mediated in part through transcriptional regulation of the FOS oncogene, and miR-196b re-expression also significantly reduced the growth of tumor xenografts. Luciferase assays demonstrated that forced expression of miR-196b inhibited the FOS promoter and AP-1 reporter activity. Finally, a case-control study revealed that methylation of miR-196b in sputum was strongly associated with lung cancer (OR = 4.7, p<0.001). Collectively, these studies highlight miR-196b as a tumor suppressor whose silencing early in lung carcinogenesis may provide a selective growth advantage to pre-malignant cells. Targeted delivery of miR-196b could therefore serve as a preventive or therapeutic strategy for the management of lung cancer.
2016-09-09 | GSE79982 | GEO
Project description:Identification of genes involved in sebaceous gland carcinoma of the eyelid
| PRJNA516871 | ENA
Project description:BMSC-derived exosomes from ovariectomized rats (OVX-Exo) and sham-operated rats (Sham-Exo) were co-cultured with bone marrow-derived macrophages to study their effects on osteoclast differentiation. Next-generation sequencing was utilized to identify the differentially expressed miRNAs (DE-miRNAs) in OVX-Exo and Sham-Exo, while target genes were analyzed using bioinformatics. The regulatory effects of miR-27a-3p and miR-196b-5p on osteogenic differentiation of BMSCs and osteoclast differentiation were verified by gain-of-function and loss-of-function analyses.Osteoclast differentiation was significantly enhanced in the OVX-Exo treatment group compared to the Sham-Exo group. Twenty DE-miRNAs were identified in OVX-Exo and Sham-Exo, among which miR-27a-3p and miR-196b-5p promoted the expressions of osteogenic genes in BMSCs. In contrast, knockdown of miR-27a-3p and miR-196b-5p increased the expressions of osteoclastic genes in osteoclasts. These 20 DE-miRNAs were found to target 11435 mRNAs. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses revealed that these target genes were involved in several biological processes and osteoporosis-related signaling pathways.
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Project description:Patients with advanced hepatocellular carcinoma (HCC) are currently treated by Sorafenib and Regorafenib but efficacy of these multikinase inhibitors is disappointing. Thus, new drugs and therapies are needed to improve HCC management in clinic. We recently reported the remarkable capacity of miR-4510 to impede the growth of HCC and hepatoblastoma cells in vitro and in vivo through GPC3 targeting and Wnt pathway inactivation (Cartier F et al, Oncotarget 2017). Here, we used a label-free proteomic approach to identify new targets of miR-4510 in HCC-deriving Huh7 cells. We transfected HCC-derived Huh7 cells with either a synthetic miR-4510 mimic or a small RNA control, extracted total proteins 24hr later and comparatively analyzed proteomes of control and miR-4510-transfected cells using a quantitative label-free approach.
2019-10-23 | PXD010085 | Pride
Project description:To identify the molecular background of eyelid sebaceous gland carcinomas (SCs), the integrated whole-exome sequencing and transcriptome sequencing for five eyelid SCs were conducted in this study.
2023-02-15 | GSE219205 | GEO