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MIR100HG regulates CALD1 gene expression by targeting miR-142-5p to affect the progress of bladder cancer cells in vitro revealed by long noncoding RNA sequencing (lncRNA and mRNA)

ABSTRACT: MIR100HG regulates CALD1 gene expression by targeting miR-142-5p to affect the progress of bladder cancer cells in vitro revealed by long noncoding RNA sequencing (lncRNA and mRNA)

PROVIDER: PRJNA771269 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16328462_1.fastq.gz	Fastqsanger.gz
	SRR16328462_2.fastq.gz	Fastqsanger.gz
	SRR16328463_1.fastq.gz	Fastqsanger.gz
	SRR16328463_2.fastq.gz	Fastqsanger.gz
	SRR16328464_1.fastq.gz	Fastqsanger.gz

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MIR100HG regulates CALD1 gene expression by targeting miR-142-5p to affect the progress of bladder cancer cells in vitro revealed by long noncoding RNA sequencing (lncRNA and mRNA)

Project description:This project completed the transcriptome analysis of 6 samples and obtained 79.158 Gb Clean Data (after quality control sequencing data). The average clean data volume of each sample was 13.193 Gb, the Q30 base percentage was over 93.02%, and the GC content was 39.35. % To 46.16%. through lncRNA sequencing, bioinformatics analysis and cell function studies, we found that MIR100HG is a new bladder cancer promoter that regulates the expression of CALD1 gene by targeting miR-142-5p and promotes the proliferation, migration and invasion of bladder cancer cells. These findings provide a new perspective for the study of the pathogenesis and development of bladder cancer, and have the potential as a new target for the diagnosis, prognosis and targeted therapy of bladder cancer.

2021-10-18 | GSE185901 | GEO

mRNA expression profile in IL-4-treated macrophages transfected with miR-142-5p ASO or miR-130a-3p mimics

2014-07-12 | GSE59347 | GEO

mRNA expression profile in IL-4-treated macrophages transfected with miR-142-5p ASO or miR-130a-3p mimics

Project description:To identify target genes of miR-142-5p and miR-130a-3p that are involved in M2 polarization, we examined the mRNA expression profile changes after altering miR-142-5p or miR-130a-3p expression in IL-4-treated macrophages. Macrophages were transfected with control ASO, miR-142-5p ASO, control mimics or miR-130-3p mimics using lentiviral vectors. After 24 hr, the cells were treated with IL-4 for 24h.mRNA was purified from total RNA after removal of rRNA (mRNA-ONLY™ Eukaryotic mRNA Isolation Kit, Epicentre). Then, each sample was amplified and transcribed into fluorescent cRNA along the entire length of the transcripts without 3’ bias utilizing a random priming method. The labeled cRNAs were hybridized onto the Human RNA Array v2.0 (8 x 60K, Arraystar). After having washed the slides, the arrays were scanned by the Agilent Scanner G2505B.

2014-07-12 | E-GEOD-59347 | biostudies-arrayexpress

Sunflower oil supplementation affects the expression of miR-20a-5p and miR-142-5p in the lactating bovine mammary gland

2016-07-01 | GSE81616 | GEO

Sunflower oil supplementation affects the expression of miR-20a-5p and miR-142-5p in the lactating bovine mammary gland

Project description:Background : In lactating cow, a sunflower oil supplementation modulated the milk composition and the mammary genes expression whose mechanisms of regulations are unclear. Results : This lipid supplementation provoke, in mammary gland, the down regulation of microRNA miR-20a-5p and miR-142-5p, which are predicted to target genes previously determined as differentially expressed including those involved in lipid metabolism. Conclusion : Those two miRNA are good candidates to explain lipogenic genes regulations after sunflower oil supplementation. Significance : The current study clarified the nutriregulation of miRNA in the mammary gland. MiRNomes obtained by NGS sequencing of mammary gland of Holstein cows at the peak of lactation received a low forage diet supplemented or not with 4% of sunflower oil were compared. MiRNA differentially expressed confirmed by RT-qPCR were related to differentially expressed genes list previously identified in the same samples.

2016-07-01 | E-GEOD-81616 | biostudies-arrayexpress

Circular RNA TMEM87A promotes cell proliferation and metastasis of gastric cancer by elevating ULK1 via sponging miR-142-5p (miRNA)

Project description:Background:Circular RNAs (circRNAs) act as vital regulators of gene expression in a variety of cancers. However, the role of circRNAs in gastric cancer (GC) remains largely unexplored. Herein, we identified that circTMEM87A sponges miR-142-5p to promote GC progression through up-regulating ULK1 expression. Methods:The expression of circTMEM87A in GC was determined by RNA sequencing and quantitative real-time PCR (qRT-PCR). The effects of knockdown or exogenous expression of circTMEM87A on GC cell phenotypes were evaluated both in vitro and in vivo. The interacting miRNA of circTMEM87A was predicted by bioinformatics and confirmed by RNA pull-down, dual-luciferase reporter assay and fluorescence in situ hybridization (FISH). The mechanism by which circTMEM87A/miR-142-5p/ULK1 axis promotes GC was determined by western blot, GFP/mRFP-LC3 puncta analysis, transmission electron microscope (TEM). Results:CircTMEM87A was dramatically elevated in GC tissues and cell lines, and high circTMEM87A expression was closely correlated with poor prognosis of GC patients. Knockdown of circTMEM87A suppressed cell growth, migration, invasion and induced apoptosis in vitro, as well as inhibited GC tumorigenicity and lung metastasis potential in vivo. Meanwhile, circTMEM87A overexpression had the opposite effects. Furthermore, we demonstrated that circTMEM87A could act as a sponge of miR-142-5p to regulate ULK1 expression and GC progression. Conclusions:Our findings suggest that circTMEM87A functions as an oncogene through the miR-142-5p/ULK1 axis in GC. CircTMEM87A might be a prognostic biomarker as well as a promising therapeutic target for GC.

2023-08-19 | GSE157015 | GEO

Circular RNA TMEM87A promotes cell proliferation and metastasis of gastric cancer by elevating ULK1 via sponging miR-142-5p (circRNA)

2023-08-19 | GSE157013 | GEO

Changes of Protein Expression after CRISPR/Cas9 Knockout of miRNA-142 in Cell Lines Derived from Diffuse large B-Cell Lymphoma // Proteome Dataset

Project description:MicroRNAs (miRNAs) post-transcriptionally regulate gene expression by inhibiting protein synthesis of target messenger RNAs (mRNAs). MicroRNA-142 (miR-142), which has tumor-suppressive properties, was functionally deleted by CRISPR/Cas9 knockout in cell lines derived from diffuse large B-cell lymphoma (DLBCL), a highly aggressive tumor that represents about 30% of non-Hodgkin lymphoma worldwide. Mutations in miR-142 affect about 20% of all cases of DLBCL. By proteome analyses, the miR-142 knockout resulted in a consistent up-regulation of 52 but also down-regulation of 41 proteins in the GC-DLBCL lines BJAB and SUDHL4. Various mitochondrial ribosomal proteins were up-regulated in line with their pro-tumorigenic properties, while proteins necessary for MHC-I presentation were down-regulated in accordance with the finding that miR-142 knockout mice have a defective immune response. Of the deregulated proteins/genes, CFL2, CLIC4, STAU1, and TWF1 are known targets of miR-142, and we could additionally confirm AKT1S1, CCNB1, LIMA1, and TFRC as new targets of miR-142-3p or -5p. We further show that seed-sequence mutations of miR-142 can be used to confirm potential targets and that miRNA knockout cell lines might thus be used to identify novel targets of miRNAs. Due to the complex contribution of miRNAs within cellular regulatory networks, in particular when a miRNA highly present in the RISC complex is deleted and can be replaced by other endogenous miRNAs, primary effects on gene expression may be covered by secondary layers of regulation

2023-03-10 | PXD037148 | Pride

microRNA-142–mediated repression of phosphodiesterase 3B critically regulates peripheral immune tolerance

Project description:Tregs play a fundamental role in immune tolerance via control of self-reactive effector T cells (Teffs). This function is dependent on maintenance of a high intracellular cAMP concentration. A number of microRNAs are implicated in the maintenance of Tregs. In this study, we demonstrate that peripheral immune tolerance is critically dependent on posttranscriptional repression of the cAMP-hydrolyzing enzyme phosphodiesterase-3b (Pde3b) by microRNA-142-5p (miR-142-5p). In this manner, miR-142-5p acts as an immunometabolic regulator of intracellular cAMP, controlling Treg suppressive function. Mir142 was associated with a super enhancer bound by the Treg lineage–determining transcription factor forkhead box P3 (FOXP3), and Treg-specific deletion of miR-142 in mice (TregΔ142) resulted in spontaneous, lethal, multisystem autoimmunity, despite preserved numbers of phenotypically normal Tregs. Pharmacological inhibition and genetic ablation of PDE3B prevented autoimmune disease and reversed the impaired suppressive function of Tregs in TregΔ142 animals. These findings reveal a critical molecular switch, specifying Treg function through the modulation of a highly conserved, cell-intrinsic metabolic pathway. Modulation of this pathway has direct relevance to the pathogenesis and treatment of autoimmunity and cancer.

2019-12-20 | GSE72279 | GEO

Gene profiling changes in BM Lin-Sca-1+c-Kit+ cells (LSKs) from miR-142-/- (KO), miR-142+/+ (WT), miR-142-/- BCR-ABL (BC CML) and miR-142+/+ BCR-ABL (CP CML) mice. [bulk RNA-Seq]

Project description:To gain insight into how miR-142 deficit drives a BC-like transformation, we performed RNA-seq on bone marrow (BM) Lin-Sca-1+c-Kit+ cells (LSKs) harvested from normal miR-142+/+ (wt) and miR-142−/− (miR-142 KO) mice, as well as from leukemic miR-142+/+ BCR-ABL (CP CML) and miR-142−/− BCR-ABL (BC CML) mice, two weeks after BCR-ABL induction. We then performed gene expression profiling analysis using data obtained from RNA-seq of 24 samples of LSK cells from 4 mouse strains (KO vs WT, KO CML vs CML).

2022-11-01 | GSE216794 | GEO

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