Identification of miR-489 or miR-504 target genes in head and neck cancer
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE19718 | GEO | 2010/01/05
SECONDARY ACCESSION(S): PRJNA121913
REPOSITORIES: GEO
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2010-01-05 | GSE19717 | GEO
Project description:We recently identified a subset of down-regulated miRNAs such as miR-145 and miR-133a in squamous cell carcinoma. Cell growth inhibitions occurred in miR-145 and miR-133a transfectants compared with the controls, suggesting that both miRNAs function as tumor suppressors. The aims of our expression studies were identification of these miRNAs target genes.
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Project description:To screen microRNAs (miRNAs) that are deregulated in head and neck squamous cell carcinoma (HNSCC), we comparatively analyzed the miRNA profiles by using 10 HNSCC patient samples and paired adjacent non-cancerous counterparts. Microarray analysis revealed that 24 miRNAs were downregulated and 19 miRNAs were elevated in HNSCC samples when compared with adjacent non-cancerous tissue. These miRNAs included upregulated miR-21-5p, miR-21-3p, and downregulated miR-99a-5p, which have been reported to regulate malignant progression of HNSCC in previous studies.
2020-01-21 | GSE124566 | GEO
Project description:Cetuximab resistance has been a major challenge for head and neck squamous cell carcinoma (HNSCC) during target therapy. Yet the mechanism that caused cetuximab resistance, especially the miRNA regulation therein remains unclear. With growing evidence suggests that miRNAs may function within the cell nucleus and act as “nuclear activating miRNAs” for targeting the promoter region or enhancers related to target genes. They are believed to regulate diseases development including tumorigenesis. This study elucidates a novel mechanism underlying cetuximab resistance in HNSCC involving the nuclear activation of KDM7A transcription via miR-451a. Herein, small RNA sequencing, qRT-PCR and FISH results provide compelling evidence of miR-451a nuclear enrichment with cetuximab treatment. ChIRP-seq, microarray, bioinformatic analysis and dual luciferase reporter assay results show that miR-451a interacts with an enhancer region in KDM7A, activating its expression and further facilitating cetuximab resistance. It is also demonstrated that activation of KDM7A by nuclear miR-451a is induced by cetuximab treatment and is AGO2 dependent. Analyses of HNSCC samples through logistic regression indicated the significance of miR-451a and KDM7A in cetuximab resistance. These discoveries hold promise for the potential utilization of miR-451a and KDM7A as valuable biomarkers for cetuximab resistance and emphasize the function of nuclear activating miRNAs.
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Project description:Cetuximab resistance has been a major challenge for head and neck squamous cell carcinoma (HNSCC) during target therapy. Yet the mechanism that caused cetuximab resistance, especially the miRNA regulation therein remains unclear. With growing evidence suggests that miRNAs may function within the cell nucleus and act as “nuclear activating miRNAs” for targeting the promoter region or enhancers related to target genes. They are believed to regulate diseases development including tumorigenesis. This study elucidates a novel mechanism underlying cetuximab resistance in HNSCC involving the nuclear activation of KDM7A transcription via miR-451a. Herein, small RNA sequencing, qRT-PCR and FISH results provide compelling evidence of miR-451a nuclear enrichment with cetuximab treatment. ChIRP-seq, microarray, bioinformatic analysis and dual luciferase reporter assay results show that miR-451a interacts with an enhancer region in KDM7A, activating its expression and further facilitating cetuximab resistance. It is also demonstrated that activation of KDM7A by nuclear miR-451a is induced by cetuximab treatment and is AGO2 dependent. Analyses of HNSCC samples through logistic regression indicated the significance of miR-451a and KDM7A in cetuximab resistance. These discoveries hold promise for the potential utilization of miR-451a and KDM7A as valuable biomarkers for cetuximab resistance and emphasize the function of nuclear activating miRNAs.
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Project description:To investigate genes regulated by miR-489, gene expression analysis was carried out between control siRNA and miR-489 mimic transfected cells.
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Project description:Current evidence implicates aberrant microRNA expression patterns in human malignancies; measurement of microRNA expression may have diagnostic and prognostic applications. Roles for microRNAs in head and neck squamous cell carcinomas (HNSCC) are largely unknown. HNSCC, a smoking-related cancer, is one of the most common malignancies worldwide but reliable diagnostic and prognostic markers have not been discovered so far. Some studies have evaluated the potential use of miRNAs as biomarkers with clinical application in HNSCC. MicroRNA expression profile of oral squamous cell carcinoma samples was determined by means of DNA microarrays. We also performed gain-of-function assays for two differentially expressed miRNAs using two squamous cell carcinoma cell lines and normal oral keratinocytes. The effect of the over-expression of these molecules was evaluated by means of global gene expression profiling and cell proliferation assessment. Altered microRNA expression was detected for a total of 72 microRNAs. Among these we found well studied molecules, such as the miR-17-92 cluster, comprising potent oncogenic miRNAs, and miR-34, recently found to interact with p53. HOX-cluster embedded miR-196a/b and miR-10b were up- and down-regulated, respectively, in tumor samples. Since validated HOX gene targets for these microRNAs are not consistently deregulated in HNSCC, we performed gain-of-function experiments, in an attempt to outline their possible role. Our results suggest that both molecules interfere in cell proliferation through distinct processes, possibly targeting a small set of genes involved in cell cycle progression.Functional data on miRNAs in HNSCC is still scarce. Our data corroborate current literature and brings new insights into the role of microRNAs in HNSCC. We also show that miR-196a and miR-10b, not previously associated with HNSCC, may play an oncogenic role in this disease through the deregulation of cell proliferation. The study of microRNA alterations in HNSCC is an essential step to the mechanistic understanding of tumor formation and could lead to the discovery of clinically relevant biomarkers.
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Project description:Diabetes promotes pro-atherogenic and pro-inflammatory phenotype of VSMC associated with vascular complications. Emerging evidence shows that miRNAs play key roles in VSMC, but their role in diabetes induced effects is unclear. We profiled novel diabetes induced miRNAs in VSMC from diabetic mice and examined their role in VSMC dysfunction. High throughput small RNA-sequencing identified 135 differentially expressed miRNAs in VSMC from type 2 diabetic db/db mice (db/dbVSMC) versus non-diabetic db/+ mice. Several of these miRNA were known to regulate VSMC functions. We further focused on miR-504, because it was highly upregulated in db/dbVSMC, but its function in VSMC is unknown. We demonstrated that miR-504 and its host gene Fgf13 were upregulated in VSMC and in vivo in aortas from db/db mice. Bioinformatics analysis predicted that miR-504 targets, including a signaling adaptor Grb10 and a transcription factor Egr2, could regulate growth factor signaling. We experimentally verified that miR-504 targets Grb10 and Egr2, and it enhanced ERK1/2 activation, proliferation and migration in VSMC. Silencing Grb10 by small interfering RNA also enhanced ERK1/2 activation, inflammatory gene expression and migration. Whereas, Egr2 silencing downregulated anti-inflammatory SOCS1 and increased inflammatory genes. Furthermore, treatment with high-glucose and palmitic acid upregulated miR-504, inhibited Grb10 and enhanced inflammatory genes in VSMC. Diabetes mis-regulates expression of several miRNAs including miR-504 involved in VSMC functions. Changes in miRNAs are sustained in non-diabetic conditions suggesting involvement of miRNA dependent mechanisms in metabolic memory implicated in vascular complications. Targeting such mechanisms could offer novel therapies strategies.
2016-04-15 | GSE74521 | GEO
Project description:Identification of miR-489 or miR-504 target genes in head and neck cancer
| PRJNA121913 | ENA