Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Long noncoding RNA Linc00673 which enhances cancer cells progression by sponging miR-515-5p to elevate expression of MARK4 in human breast cancer

ABSTRACT: Long noncoding RNA Linc00673 which enhances cancer cells progression by sponging miR-515-5p to elevate expression of MARK4 in human breast cancer

PROVIDER: PRJNA551136 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9602290.fastq.gz	Fastqsanger.gz
	SRR9602281.fastq.gz	Fastqsanger.gz
	SRR9602283.fastq.gz	Fastqsanger.gz
	SRR9602284.fastq.gz	Fastqsanger.gz
	SRR9602285.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 9

Similar Datasets

Long noncoding RNA Linc00673 which enhances cancer cells progression by sponging miR-515-5p to elevate expression of MARK4 in human breast cancer

Project description:In the present study, Linc00673 displayed high expression in breast cancer tissues and was associated with poor prognosis of breast cancer patients. Importantly, Linc00673 depletion inhibited breast cancer cell proliferation by impairing cell cycle progression and apoptosis. Mechanically, RNA sequencing was performed to investigate the potential crosstalk between Linc00673 and its targets. We found that Linc00673 acted as a competing endogenous RNA by sponging miR-515-5p to regulate MARK4 expression which inhibits the Hippo signaling pathway to promote proliferation of breast cancer.

2019-10-29 | GSE133331 | GEO

miR-515-5p suppresses trophoblast cell invasion and proliferation through XIAP regulation in preeclampsia

Project description:MicroRNAs (miRNAs) are non-coding small RNA molecules that can be secreted into the circulation and which exist in remarkably stable forms. Circulating miRNAs regulates numerous regulations of biological process and aberrantly expressed in pathological status. Differentially expressed circulating miRNAs have received attention as potential biomarkers for many diseases. In this study, we revealed that miR-515-5p was significantly upregulated in maternal serum from preeclampsia (PE) patients in comparison to normal pregnant women. Bioinformatics prediction and a dual-luciferase reporter gene assay revealed that miR-515-5p directly targets the X-linked inhibitor of apoptosis protein (XIAP) 3’-untranslated region (UTR). Furthermore, the XIAP mRNA expression was decreased in the preeclamptic placenta in comparison to that in normal pregnancy. The overexpression of miR-515-5p inhibited the proliferation and invasion of HTR-8/SVneo trophoblast cells. Collectively, miR-515-5p may play critical roles in the pathogenesis of PE through suppression of the expression of XIAP and serum miR-515-5p may act as a potential biomarker for PE

2022-06-26 | GSE206763 | GEO

Silenced LINC01963 enhanced the chemosensitivity of prostate cancer cells to docetaxel by sponging miR-216b-5p to inhibit TrkB protein level

Project description:Long noncoding RNAs (lncRNAs) affect docetaxel chemosensitivity. However, the biological role and regulatory mechanisms of lncRNAs in docetaxel-resistant prostate cancer remain unclear. Differences in lncRNAs were evaluated by lncRNA sequencing and evaluated using quantitative real-time polymerase chain reaction, and TrkB expression was measured through Western blot analysis. Proliferation was measured using the MTS, while apoptosis and cell cycle were measured using flow cytometry. Additionally, migration and invasion were measured using transwell assays. Forty-eight female BALB/c nude mice were used for subcutaneous tumorigenicity and lung metastasis assays. We found that LINC01963 was overexpressed in the PC3-DR cells. LINC01963 silencing enhanced the chemosensitivity of PC3-DR to docetaxel and inhibited tumorigenicity and lung metastasis, while LINC01963 overexpression enhanced the chemoresistance of PC3 cells to docetaxel. It was found that LINC01963 sponges miR-216b-5p. The miR-216b-5p inhibitor reversed the suppressive effect of sh-LINC01963 on PC3-DR cell proliferation, migration, and invasion. Furthermore, miR-216b-5p can bind to the 3’-UTR of NTRK2 and inhibit TrkB protein levels. TrkB enhances docetaxel resistance in prostate cancer and reverses the effects of LINC01963 silencing and miR-216b-5p overexpression. In conclusion, silencing LINC01963 enhanced the chemosensitivity of PC3-DR to docetaxel by sponging miR-216b-5p to inhibit TrkB protein levels.

2021-12-13 | GSE190648 | GEO

lncRNA n384546 promotes thyroid papillary cancer proliferation and migration by targeting miR-145-5p to regulate AKT3

Project description:we document a novel lncRNA, n384546, which may exert its oncogenic property in PTC tumorigenesis by sponging miR-145-5p and then regulating its target AKT3.This study reveals that n384546 is an oncogenic lncRNA in human thyroid cancer.

2019-06-16 | GSE124841 | GEO

CircSry regulates spermatogenesis by enhancing γH2AX expression via sponging miR138-5p

Project description:CircSry regulates spermatogenesis by enhancing γH2AX expression via sponging miR138-5p

| PRJNA767879 | ENA

Circ_0000235 Targets MCT4 to Promote Glycolysis and Progression of Bladder Cancer by Sponging miR-330-5p

Project description:Circ_0000235 Targets MCT4 to Promote Glycolysis and Progression of Bladder Cancer by Sponging miR-330-5p

| PRJNA978602 | ENA

Circ_0000235 Targets MCT4 to Promote Glycolysis and Progression of Bladder Cancer by Sponging miR-330-5p

Project description:Warburg effect plays a crucial role in bladder cancer (Bca) development. However, the mechanism by which glycolysis is involved in Bca remains poorly understood. CircRNAs commonly play a regulatory role in tumor progression. Our study discovered and identified a novel circRNA, hsa_circ_0000235 (circ235), and investigated its role in the glycolytic process, which further results in the progression of Bca. We applied qRT-PCR to assess its clinicopathological relevance and evaluated its proliferation, migration, and glycolytic capacity. We investigated its mechanism using RNA immunoprecipitation, dual-luciferase reporters, and fluorescence in situ hybridization. The findings demonstrated that circ235 was dramatically increased in Bca tissues and was related to a worse prognosis. In vitro studies revealed that circ235 accelerated the rate of extracellular acidification and promoted glucose uptake and lactate manufacture in Bca cells. Additionally, it strengthened the capacity of Bca cells to proliferate and migrate. Experiments on animals revealed that downregulating circ235 dramatically reduced carcinogenesis and tumor growth. Cir235 activates monocarboxylate transporter 4 (MCT4) by sponging miR-330-5p, which promotes glycolysis and tumor growth. In conclusion, these findings imply that circ235 may be a viable molecular marker and therapeutic site for Bca.

2023-08-09 | GSE233933 | GEO

Effect of miRNA-30e-5p on innate immunity during viral infection.

Project description:Comparative transcriptomic analysis of A549 cell after overexpression of miRNA-30e-5p revealed that miRNA-30e-5p elevate innate immune responses by targeting the negative regulators of innate immune signalling.

2020-07-27 | GSE130005 | GEO

miR-515-5p suppresses trophoblast cell invasion and proliferation through XIAP regulation in preeclampsia

Project description:miR-515-5p suppresses trophoblast cell invasion and proliferation through XIAP regulation in preeclampsia

| PRJNA852084 | ENA

miR-1307-5p counteracts breast cancer angiogenesis and metastasis

Project description:MiRNAs have been shown to alter both protein expression and secretion in different cellular contexts. By combining in vitro, in vivo and in silico techniques, we demonstrated that overexpression of pre-miR-1307 reduced the ability of breast cancer cells to induce endothelial cell sprouting and angiogenesis. However, the molecular mechanism behind this and the effect of the individual mature miRNAs derived from pre-miR-1307 on protein secretion and is largely unknown. Here, we overexpressed miR-1307-3p|0, -3p|1 and 5p|0 in MDA-MB-231 breast cancer cells and assessed the impact of miRNA overexpression on protein secretion by Mass Spectrometry. Unsupervised hierarchical clustering revealed a distinct phenotype induced by overexpression of miR-1307-5p|0 compared to the controls and to the 5’isomiRs derived from the 3p-arm. Together, our results suggest different impacts of miR-1307-3p and miR-1307-5p on protein secretion which is in line with our in vitro observation that miR-1307-5p, but not the isomiRs derived from the 3p-arm reduce endothelial cell sprouting in vitro. Hence these data support the hypothesis that miR-1307-5p is at least partly responsible for impaired vasculature in tumors overexpressing pre-miR-1307.

2024-12-11 | PXD041087 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data