Transcriptome analysis of control and MALAT1 lncRNA-depleted RNA samples from human diploid lung fibroblasts [WI38]
Long noncoding RNA MALAT1 controls cell cycle progression by regulating the expression of oncogenic transcription factor B-MYB.
Specimen part, Cell line
View SamplesLong non-coding RNAs (lncRNAs) regulate vital biological processes, including cell proliferation, differentiation and development. A subclass of lncRNAs is synthesized from microRNA host genes (MIRHGs) due to pre-miRNA processing, and is categorized as miRNA-host gene lncRNAs (lnc-miRHGs). Presently, it is not clear whether lnc-miRHG perform additional functions. We demonstrate a miRNA-independent role for a nuclear-enriched lnc-miRHG in cell cycle progression. MIR100HG produces spliced and stable lncRNAs (lnc-MIR100HG) that display elevated levels during the G1 phase of the cell cycle. Depletion of lnc-MIR100HG in human cells results in aberrant cell cycle progression with out altering the levels of miRNA encoded within MIR100HG. Notably, lnc-MIR100HG interacts with the HuR/Elav as well as with several of HuR-target mRNAs. Further, lnc-MIR100HG-depleted cells show reduced interaction between HuR and its target mRNAs, indicating that lnc-MIR100HG facilitates interaction between HuR and target mRNAs. Our studies have unearthed novel roles played by miRHG-encoded lncRNAs in regulating RNA binding protein activity, thereby underscoring the importance of determining the function of several hundreds of miRHG lncRNAs that are present in human genome.
MIR100 host gene-encoded lncRNAs regulate cell cycle by modulating the interaction between HuR and its target mRNAs.
Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Malat1 is not an essential component of nuclear speckles in mice.
Age, Specimen part
View SamplesMalat1 is an abundant long noncoding RNA that localizes to nuclear bodies known as nuclear speckles, which contain a distinct set of pre-mRNA processing factors. Previous in vitro studies have demonstrated that Malat1 interacts with pre-mRNA splicing factors, including the serine- and arginine-rich (SR) family of proteins, and regulates a variety of biological processes, including cancer cell migration, synapse formation, cell cycle progression, and responses to serum stimulation. To address the physiological function of Malat1 in a living organism, we generated Malat1-KO (KO) mice using homologous recombination. Unexpectedly, the Malat1-KO mice were viable and fertile, showing no apparent phenotypes. Nuclear speckle markers were also correctly localized in cells that lacked Malat1. However, the cellular levels of another long noncoding RNA, Neat1, which is an architectural component of nuclear bodies known as paraspeckles, were downregulated in a particular set of tissues and cells lacking Malat1.
Malat1 is not an essential component of nuclear speckles in mice.
Specimen part
View SamplesIn order to study the transcriptional response of the fly brain to sugar and complete starvation, we first confirmed that 24 hours of sugar and complete starvation in flies is sufficient to elicit a homeostatic response. Subsequently, we used holidic medium to study effects of deficiency of a specfic macronutrient- cabohydrate in the food. To do so , we generated RNA- seq libraries from brains of 5 day old mated adult male flies maintained on different feeding regimes and used the sequencing data to identify diffrentially expressed genes in the brain under different feeding regimes. Overall design: For each condition, we used RNA prepared from 120-130 manually dissected adult fly brains maintained under complete starvation or sugar starvation regime for 24 hours.
Sugar Promotes Feeding in Flies via the Serine Protease Homolog scarface.
Sex, Specimen part, Cell line, Subject
View SamplesWe report that AUF1 modulates global mRNA stability and translation, in turn promoting the maintenance of DNA integrity. Overall design: Please see individual series. For AUF1 PAR-CLIP, the four isoforms of AUF1 (p37, p40, p42, and p45) tagged with a Flag epitope were expressed in HEK293 cells. For total RNA-Seq HEK293 cells were transfected with Control siRNA, AUF1 siRNA, Empty Vector, Flag-AUF1 p37, p40, p42, or p45 as well as WI-38 cells were collected at PDL 15 and 55 and also transfected with Control siRNA, AUF1 siRNA, HuR siRNA. For Ribo-Seq HeLa cells were transfected with Control siRNA, AUF1 siRNA, or HuR siRNA.
PAR-CLIP analysis uncovers AUF1 impact on target RNA fate and genome integrity.
No sample metadata fields
View SamplesWe report that AUF1 modulates global mRNA stability and translation, in turn promoting the maintenance of DNA integrity. Overall design: Please see individual series. In short, for AUF1 PAR-CLIP, the four isoforms of AUF1 (p37, p40, p42, and p45) tagged with a Flag epitope were expressed in HEK293 cells. For total RNA-Seq HEK293 cells were transfected with Control siRNA, AUF1 siRNA, Empty Vector, Flag-AUF1 p37, p40, p42, or p45 as well as WI-38 cells were collected at PDL 15 and 55 and also transfected with Control siRNA, AUF1 siRNA, HuR siRNA. For Ribo-Seq HeLa cells were transfected with Control siRNA, AUF1 siRNA, or HuR siRNA.
PAR-CLIP analysis uncovers AUF1 impact on target RNA fate and genome integrity.
No sample metadata fields
View SamplesMicroRNAs have been implicated in various skin cancers, including melanoma, squamous cell carcinoma, and basal cell carcinoma; however, the expression of microRNAs and their role in Merkel cell carcinoma (MCC) have yet to be explored in depth. To identify microRNAs specific to MCC (MCC-miRs), next-generation sequencing (NGS) of small RNA libraries was performed on different tissue samples including MCCs, other cutaneous tumors, and normal skin. Comparison of the profiles identified several microRNAs upregulated and downregulated in MCC. For validation, their expression was measured via qRT-PCR in a larger group of MCC and in a comparison group of non-MCC cutaneous tumors and normal skin. Eight microRNAs were upregulated in MCC: miR-502-3p, miR-9, miR-7, miR-340, miR-182, miR-190b, miR-873, and miR-183. Three microRNAs were downregulated: miR-3170, miR-125b, and miR-374c. Many of these MCC-miRs, with the miR-183/182/96a cistron in particular, have connections to tumorigenic pathways implicated in MCC pathogenesis. In situ hybridization confirmed that the highly expressed MCC-miR, miR-182, is localized within tumor cells. Furthermore, NGS and qRT-PCR reveals that several of these MCC-miRs are highly expressed in the patient-derived MCC cell line, MS-1. These data indicate that we have identified a set of MCC-miRs with high implications for MCC research. Overall design: To identify microRNAs specific to Merkel cell carcinoma (MCC) next-generation sequencing (NGS) of small RNA libraries was performed on different tissue samples including MCCs, other cutaneous tumors, and normal skin
Characterization of the Merkel Cell Carcinoma miRNome.
No sample metadata fields
View SamplesGene expression profile of laser-capture microdissected epithelium component of 6 mucinous cystic neoplasms of the pancreas were included in the study. The expression arrays were generated with Affymetrix HU133A gene chips (18,462 genes/EST transcripts).
Characterization of gene expression in mucinous cystic neoplasms of the pancreas using oligonucleotide microarrays.
Sex, Specimen part, Disease, Subject
View SamplesTobacco exposure has been established to be a major risk factor for developing oral squamous cell carcinoma (OSCC). The purpose of this study is to identify potential biomarkers to distinguish the biological effectsof combustible tobacco products from that of non-combustible tobacco products using normal human gingival epithelial cells (HGEC), non-metastatic (101A) and metastatic (101B) OSCC cell lines.
AKR1C1 as a Biomarker for Differentiating the Biological Effects of Combustible from Non-Combustible Tobacco Products.
Cell line
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