Epigenetic silencing of noncoding RNA nc886 provokes oncogenes during esophageal tumorigenesis
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE51732 | GEO | 2013/10/31
SECONDARY ACCESSION(S): PRJNA224722
REPOSITORIES: GEO
Similar Datasets
Project description:nc886 is a 101 nucleotides long non-coding RNA that is also known as a precursor microRNA or a vault RNA. nc886 has been suggested to be a tumor suppressor, mainly inferred by its expression pattern as well as its genomic location at human chromosome 5q31, a locus for a tumor suppressor gene(s). Pre-clinical study In order to understand potential roles of nc886 in esophageal squamous cell carcinoma (ESCC), we performed the knockdown of nc886 in nonmalignant HET-1A cells and ESCC cell lines (TE-1 and TE-8) and identified and analyzed genes whose expression is activated by nc886 knockdown in ESCC.
2013-10-31 | E-GEOD-51732 | biostudies-arrayexpress
Project description:nc886 is a 101 nucleotides long non-coding RNA that is also known as a precursor microRNA or a vault RNA. nc886 has been suggested to be a tumor suppressor, mainly inferred by its expression pattern as well as its genomic location at human chromosome 5q31, a locus for a tumor suppressor gene(s). In order to understand potential roles of nc886 in gastric cancer, we performed the knockdown of nc886 in nonmalignant HFE-145 cells and identified and analyzed genes whose expression is activated by nc886 knockdown in gastric cancer.
2015-09-30 | GSE51067 | GEO
Project description:Targeted cancer therapy for squamous cell carcinoma (SCC) has made little progress largely due to a lack of knowledge of the driving genomic alterations. Small non-coding RNAs (sncRNAs) as a potential biomarker and therapeutic target to SCC remain a challenge. We analyzed sncRNAs microarray in 108 fresh frozen specimens of esophageal squamous cell carcinoma (ESCC) as discovery set and assessed associations between sncRNAs and recurrence-free survival. SncRNA signature identified was externally validated in two independent cohorts. We investigated the functional consequences of sncRNA identified and its integrative analysis of complex cancer genomics. We identified 3 recurrence-associated sncRNAs (miR-223, miR-1269a and nc886) from discovery set and proved risk prediction model externally in high and low volume centers. We uncovered through in vitro experiment that nc886 was down-regulated by hypermethylation of its promoter region and influences splicing of pre-mRNAs with minor introns by regulating expression of minor spliceosomal small nuclear RNAs (snRNAs) such as RNU4atac. Integrative analysis from lung SCC data in The Cancer Genome Atlas revealed that patients with lower expression of nc886 had more genetic alterations of TP53, DNA damage response and cell cycle genes. nc886 inhibits minor splicing to suppress expression of certain oncogenes such as PARP1 and E2F family containing minor introns. We present risk prediction model with sncRNAs for ESCC. Among them, nc886 may contribute to complete minor splicing via regulation of minor spliceosomal snRNAs supporting the notion that aberrant alteration in minor splicing might be a key driver of ESCC. Pre-clinical study Analysis of Esophageal Squamous Cell Carcinoma cell lines knocked-down for nc886 and vault RNA VTRNA1-1 via antisense oligonucleotide (ASO)-targeting.
2016-06-30 | E-GEOD-55854 | biostudies-arrayexpress
Project description: Not available
| S-EPMC4116496 | biostudies-literature
Project description:Targeted cancer therapy for squamous cell carcinoma (SCC) has made little progress largely due to a lack of knowledge of the driving genomic alterations. Small non-coding RNAs (sncRNAs) as a potential biomarker and therapeutic target to SCC remain a challenge. We analyzed sncRNAs microarray in 108 fresh frozen specimens of esophageal squamous cell carcinoma (ESCC) as discovery set and assessed associations between sncRNAs and recurrence-free survival. SncRNA signature identified was externally validated in two independent cohorts. We investigated the functional consequences of sncRNA identified and its integrative analysis of complex cancer genomics. We identified 3 recurrence-associated sncRNAs (miR-223, miR-1269a and nc886) from discovery set and proved risk prediction model externally in high and low volume centers. We uncovered through in vitro experiment that nc886 was down-regulated by hypermethylation of its promoter region and influences splicing of pre-mRNAs with minor introns by regulating expression of minor spliceosomal small nuclear RNAs (snRNAs) such as RNU4atac. Integrative analysis from lung SCC data in The Cancer Genome Atlas revealed that patients with lower expression of nc886 had more genetic alterations of TP53, DNA damage response and cell cycle genes. nc886 inhibits minor splicing to suppress expression of certain oncogenes such as PARP1 and E2F family containing minor introns. We present risk prediction model with sncRNAs for ESCC. Among them, nc886 may contribute to complete minor splicing via regulation of minor spliceosomal snRNAs supporting the notion that aberrant alteration in minor splicing might be a key driver of ESCC. Clinical study ESCC tumor samples vs. ESCC normal samples
2016-06-30 | E-GEOD-55856 | biostudies-arrayexpress
Project description:Targeted cancer therapy for squamous cell carcinoma (SCC) has made little progress largely due to a lack of knowledge of the driving genomic alterations. Small non-coding RNAs (sncRNAs) as a potential biomarker and therapeutic target to SCC remain a challenge. We analyzed sncRNAs microarray in 108 fresh frozen specimens of esophageal squamous cell carcinoma (ESCC) as discovery set and assessed associations between sncRNAs and recurrence-free survival. SncRNA signature identified was externally validated in two independent cohorts. We investigated the functional consequences of sncRNA identified and its integrative analysis of complex cancer genomics. We identified 3 recurrence-associated sncRNAs (miR-223, miR-1269a and nc886) from discovery set and proved risk prediction model externally in high and low volume centers. We uncovered through in vitro experiment that nc886 was down-regulated by hypermethylation of its promoter region and influences splicing of pre-mRNAs with minor introns by regulating expression of minor spliceosomal small nuclear RNAs (snRNAs) such as RNU4atac. Integrative analysis from lung SCC data in The Cancer Genome Atlas revealed that patients with lower expression of nc886 had more genetic alterations of TP53, DNA damage response and cell cycle genes. nc886 inhibits minor splicing to suppress expression of certain oncogenes such as PARP1 and E2F family containing minor introns. We present risk prediction model with sncRNAs for ESCC. Among them, nc886 may contribute to complete minor splicing via regulation of minor spliceosomal snRNAs supporting the notion that aberrant alteration in minor splicing might be a key driver of ESCC. Clinical study ESCC tumor samples.
2016-06-30 | E-GEOD-66258 | biostudies-arrayexpress
Project description:Targeted cancer therapy for squamous cell carcinoma (SCC) has made little progress largely due to a lack of knowledge of the driving genomic alterations. Small non-coding RNAs (sncRNAs) as a potential biomarker and therapeutic target to SCC remain a challenge. We analyzed sncRNAs microarray in 108 fresh frozen specimens of esophageal squamous cell carcinoma (ESCC) as discovery set and assessed associations between sncRNAs and recurrence-free survival. SncRNA signature identified was externally validated in two independent cohorts. We investigated the functional consequences of sncRNA identified and its integrative analysis of complex cancer genomics. We identified 3 recurrence-associated sncRNAs (miR-223, miR-1269a and nc886) from discovery set and proved risk prediction model externally in high and low volume centers. We uncovered through in vitro experiment that nc886 was down-regulated by hypermethylation of its promoter region and influences splicing of pre-mRNAs with minor introns by regulating expression of minor spliceosomal small nuclear RNAs (snRNAs) such as RNU4atac. Integrative analysis from lung SCC data in The Cancer Genome Atlas revealed that patients with lower expression of nc886 had more genetic alterations of TP53, DNA damage response and cell cycle genes. nc886 inhibits minor splicing to suppress expression of certain oncogenes such as PARP1 and E2F family containing minor introns. We present risk prediction model with sncRNAs for ESCC. Among them, nc886 may contribute to complete minor splicing via regulation of minor spliceosomal snRNAs supporting the notion that aberrant alteration in minor splicing might be a key driver of ESCC.
2016-06-30 | GSE55856 | GEO
Project description:Targeted cancer therapy for squamous cell carcinoma (SCC) has made little progress largely due to a lack of knowledge of the driving genomic alterations. Small non-coding RNAs (sncRNAs) as a potential biomarker and therapeutic target to SCC remain a challenge. We analyzed sncRNAs microarray in 108 fresh frozen specimens of esophageal squamous cell carcinoma (ESCC) as discovery set and assessed associations between sncRNAs and recurrence-free survival. SncRNA signature identified was externally validated in two independent cohorts. We investigated the functional consequences of sncRNA identified and its integrative analysis of complex cancer genomics. We identified 3 recurrence-associated sncRNAs (miR-223, miR-1269a and nc886) from discovery set and proved risk prediction model externally in high and low volume centers. We uncovered through in vitro experiment that nc886 was down-regulated by hypermethylation of its promoter region and influences splicing of pre-mRNAs with minor introns by regulating expression of minor spliceosomal small nuclear RNAs (snRNAs) such as RNU4atac. Integrative analysis from lung SCC data in The Cancer Genome Atlas revealed that patients with lower expression of nc886 had more genetic alterations of TP53, DNA damage response and cell cycle genes. nc886 inhibits minor splicing to suppress expression of certain oncogenes such as PARP1 and E2F family containing minor introns. We present risk prediction model with sncRNAs for ESCC. Among them, nc886 may contribute to complete minor splicing via regulation of minor spliceosomal snRNAs supporting the notion that aberrant alteration in minor splicing might be a key driver of ESCC.
2016-06-30 | GSE55854 | GEO
Project description:Targeted cancer therapy for squamous cell carcinoma (SCC) has made little progress largely due to a lack of knowledge of the driving genomic alterations. Small non-coding RNAs (sncRNAs) as a potential biomarker and therapeutic target to SCC remain a challenge. We analyzed sncRNAs microarray in 108 fresh frozen specimens of esophageal squamous cell carcinoma (ESCC) as discovery set and assessed associations between sncRNAs and recurrence-free survival. SncRNA signature identified was externally validated in two independent cohorts. We investigated the functional consequences of sncRNA identified and its integrative analysis of complex cancer genomics. We identified 3 recurrence-associated sncRNAs (miR-223, miR-1269a and nc886) from discovery set and proved risk prediction model externally in high and low volume centers. We uncovered through in vitro experiment that nc886 was down-regulated by hypermethylation of its promoter region and influences splicing of pre-mRNAs with minor introns by regulating expression of minor spliceosomal small nuclear RNAs (snRNAs) such as RNU4atac. Integrative analysis from lung SCC data in The Cancer Genome Atlas revealed that patients with lower expression of nc886 had more genetic alterations of TP53, DNA damage response and cell cycle genes. nc886 inhibits minor splicing to suppress expression of certain oncogenes such as PARP1 and E2F family containing minor introns. We present risk prediction model with sncRNAs for ESCC. Among them, nc886 may contribute to complete minor splicing via regulation of minor spliceosomal snRNAs supporting the notion that aberrant alteration in minor splicing might be a key driver of ESCC.
2016-06-30 | GSE66258 | GEO
Project description:Understanding of molecular system how tumor-suppressor p53 selectively activates and/or completes appropriate tumor-suppressor pathway in response to various stresses is still one of the most important issues to be clarified. We analyzed a molecular mechanism for the completion of p53-dependent ribosome stress responsible pathway by miR-101. To this end, expression microarray analyses were conducted in the presence or absence of miR-101. We found that miR-101 induces the activation of p53-dependent G2 phase cell cycle arrest through the increased phosphorylation of ATM, leading to the p53-depdent apoptosis.
2017-08-16 | GSE85696 | GEO