Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA369400 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5220020.fastq.gz | Fastqsanger.gz | |||
| SRR5220021.fastq.gz | Fastqsanger.gz | |||
| SRR5220022.fastq.gz | Fastqsanger.gz | |||
| SRR5220023.fastq.gz | Fastqsanger.gz | |||
| SRR5220024.fastq.gz | Fastqsanger.gz |
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Project description:we profiled small RNAs binding to phosphorylated Serine (p-Ser), Threonine (p-Thr) and Tyrosine (p-Tyr) residues of proteins in human lung bronchial epithelial (HBE) and lung squamous cell carcinoma (SCC) cells. A total of 1986 unique p-Proteins interacted piRNAs and piRNA-Likes were called.
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Project description:PIWI-interacting RNAs (piRNAs) are thought to silence transposon and gene expression during development. However, the roles of piRNAs in somatic tissues are largely unknown. Here we report the identification of 555 piRNAs in human lung bronchial epithelial (HBE) and non-small cell lung cancer (NSCLC) cell lines, including 295 that don’t exist in databases termed as piRNA-Like sncRNAs or piRNA-Ls. Distinctive piRNA/piRNA-L expression patterns are observed between HBE and NSCLC cells. piRNA-L-163 (piR-L-163), the top down-regulated piRNA-L in NSCLC cells, binds directly to phosphorylated ERM proteins (p-ERM), which is dependent on the central part of UUNNUUUNNUU motif in piR-L-163 and the RRRKPDT element in ERM, and. The piR-L-163/p-ERM interaction is critical for p-ERM’s binding capability to filamentous actin (F-actin) and ERM-binding phosphoprotein 50 (EBP50). Thus, piRNA/piRNA-L may play a regulatory role through direct interaction with proteins in physiological and pathophysiological conditions.
2015-09-03 | PXD002076 | Pride
Project description:To elucidate potential roles of piRNA in lung cancer, we analyzed global piRNA expression profiles in 8 NSCLC and 3 HBE cell lines. RNA-seq results showed that >99% of the approximately 4.5 million reads were between 26 and 32 bases. Most of the piRNA loci are represented by two or more identical reads. We observed a total 555 expressed mature piRNAs, distributed among chromosomes and mitochondria with bias in chromosomes 1 and 6. 99% of the piRNAs are mapped to intergenic regions (64%) or introns (35%) and 1% to exons. Of the 555 mature piRNAs, 260 (47%) have been recorded in NCBI whereas 295 (53%) are novel. These results provide a comprehensive view of piRNA expressed in human bronchial epithelial cells and NSCLC cells. To get the purified mature piRNAs, small RNA (<200nt) was separated from total RNAs firstly, and then piRNA were purified in one nucleotide resolution gel. A unique 6 nt barcode for every cell line to distinguish each reads from each specific cell line, and the right size of small RNAs were used library for Illumina sequencing.
2016-06-27 | E-GEOD-57681 | biostudies-arrayexpress
Project description:To elucidate potential roles of piRNA in lung cancer, we analyzed global piRNA expression profiles in 8 NSCLC and 3 HBE cell lines. RNA-seq results showed that >99% of the approximately 4.5 million reads were between 26 and 32 bases. Most of the piRNA loci are represented by two or more identical reads. We observed a total 555 expressed mature piRNAs, distributed among chromosomes and mitochondria with bias in chromosomes 1 and 6. 99% of the piRNAs are mapped to intergenic regions (64%) or introns (35%) and 1% to exons. Of the 555 mature piRNAs, 260 (47%) have been recorded in NCBI whereas 295 (53%) are novel. These results provide a comprehensive view of piRNA expressed in human bronchial epithelial cells and NSCLC cells.
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Project description:mature piRNAs expression profile in human bronchial epithelial (HBE) and non-small cell lung cancer (NSCLC) cells
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Project description:Chronic obstructive pulmonary disease (COPD) and squamous cell lung carcinoma (SCC) are both smoking-related diseases. Interestingly, COPD itself is a risk factor for SCC, and this is independent of smoking history. Inferring from this knowledge, it is plausible to assume that patients with COPD may have a different gene expression profile in normal bronchial epithelium and in SCC. To test this hypothesis, we compared gene expression profiles in bronchial epithelium and in SCC from patients with and without COPD. Gene expression profiles were generated using whole human genome oligo microarrays for 28 laser microdissected histologically normal bronchial epithelium samples (10 without COPD, 18 with COPD) and 35 laser microdissected SCC samples (17 without COPD, 18 with COPD). We found no significant differences in gene expression levels between normal bronchial epithelium from patients with and without COPD. Remarkably, 374 genes were differentially expressed in SCC obtained from patients with or without COPD; 295 showed a higher expression level in SCC from patients with COPD and 79 genes showed higher expression levels in SCC from patients without COPD. Genes related to mitochondrial localization (n=44) and genes located on chromosomal arm 5q (n=34) were significantly overrepresented. For both categories, all genes showed a higher expression level in SCC from patients with COPD than from those without COPD. In conclusion, SCC from patients with COPD show a different gene expression profile compared to SCC from patients without COPD. This suggests that COPD related factors affect the gene expression signature in SCC.
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2008-10-01 | GSE12428 | GEO
Project description:Lung cancer is the leading cause of cancer death in USA. Squamous Cell Carcinoma (SCC) is one of the subtypes of lung cancer. It is still largely unknown which genes or pathways regulate lung SCC development. Recently, we found JNK1/2 pathway was inhibited in mouse lung SCC induced by double ablation of Pten and Lkb1 in mouse lung epithelial cells. Now we aim to identify a genome-wide molecular signature of JNK1/2 signaling in mouse squamous cell carcinoma cells and determine pathways that transduce JNK1/2 signaling.
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Project description:We comprehensively characterized the gene expression alterations occurring during squamous lung cancer development. Fresh frozen human bronchial biopsies (N=122) at successive morphological stages of lung squamous carcinogenesis were obtained by fluorescence bronchoscopy and analyzed using gene expression microarrays. A total of 122 biopsies from 77 individuals, 35 former and 42 current smokers, were included. The 122 biopsies were distributed according to histology and fluorescence status as follows: 13 biopsies with normal histology and normofluorescent (8/5 biopsies from former/current smokers), 14 with normal histology and hypofluorescent (8/6), 15 hyperplasia (7/8), 15 metaplasia (5/10), 13 mild dysplasia (8/5), 13 moderate dysplasia (7/6), 12 severe dysplasia (2/10), 13 carcinoma in situ (5/8) and 14 squamous cell carcinoma (SCC, 5/9). In addition, normal bronchial biopsies from 16 never-smokers were collected and pooled for use as reference RNA.
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Project description:PIWI-interacting RNAs (piRNAs) are genomically-encoded small RNAs that regulate germ cell development and guarantee germline integrity. Mature piRNAs engage Piwi Argonaute proteins to silence complementary transcripts, including transposable elements and endogenous genes. To date, piRNA biogenesis mechanisms are still unclear. Here, we show that the RNA Polymerase II subunit RPB-9 is required to promote transcription elongation at piRNA loci. Through genetic and biochemical experiments, we demonstrate that rpb-9-mediated piRNA production is needed to repress two DNA transposon families and a subset of somatic genes in the C. elegans germline.
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