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MiR-214-3p overexpression inhibits apoptotsis during induction of breast cancer

ABSTRACT: miR-214-3p overexpression inhibits apoptotsis during induction of breast cancer

PROVIDER: PRJNA784942 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17074302_1.fastq.gz	Fastqsanger.gz
	SRR17074302_2.fastq.gz	Fastqsanger.gz
	SRR17074303_1.fastq.gz	Fastqsanger.gz
	SRR17074303_2.fastq.gz	Fastqsanger.gz
	SRR17074304_1.fastq.gz	Fastqsanger.gz

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miR-214-3p overexpression inhibits apoptotsis during induction of breast cancer

Project description:We treated horse mammary derived epithelial cells (MDECs) with either a miR-214-3p mimic or a negative mimic control in the presence of the carcinogenic agent DMBA. Over expression of miR-214-3p suppressed cell apoptosis compared to the control, and suggests a potential oncogenic role in breast cancer.

2023-10-11 | GSE189879 | GEO

miR-214-3p inhibits SiO₂-induced macrophage inflammation and attenuates pulmonary fibrosis by targeting Bim in silicosis

Project description:Silicosis is a devastating occupational lung disease characterized by chronic inflammation and diffuse interstitial fibrosis. Previous studies have shown that miRNA imbalance contributes to silicosis progression, however, the role of miR-214-3p in silicosis is largely unknown. In this study, we performed proteomics analysis of macrophage transfected with miR-NC or miR-214-3p after silica dust exposure for 36 hours, to analyze the effect of miR-214-3p overexpression on SiO2-induced macrophage inflammation.

2025-06-10 | PXD064802 |

Impact of miR-199-5p, miR-199a-3p and miR-214-3p overexpression on human lung fibroblasts

Project description:To identify putative novel specific targets of miR-199-5p, miR-199a-3p and miR-214-3p, we overexpressed these miRNAs in human MRC5 pulmonary fibroblasts (CCL-171) using synthetic pre-miRNAs or a synthetic “negative” pre-miRNA control (miR-Neg). RNA samples were harvested 48 hours post-transfection and 3 independent experiments were carried out.

2019-04-11 | GSE97824 | GEO

Comprehensive long-read transcriptomic analysis reveals multi-level transcriptional alterations mediated by miR-214-3p dysregulation in gastric cancer cells

Project description:Long-length sequencing has been widely used in cancer-related research for exploring transcriptome variations in human cancer in recent years. miR-214-3p, a microRNA, has been reported to have abnormal expression and play important regulation roles in diverse cancers. However, information about the genome-wide targets and action mechanisms of miR-214-3p in cancer cells is still limited. Here, long-read sequencing were performed to character the transcriptome variations after disturbing the expression of miR-214-3p in AGS cells, a gastric cancer cell line. The results showed that both miR-214-3p overexpression (OE) and suppression (KD) extensively increased or decreased expression level of a number of genes involved in apoptotic process and transcription at transcript level and gene level. In particular, both miR-214-3p KD and OE could increase or decrease on the expression levels of some target genes at the same direction. Moreover, miR-214-3p broadly regulated the alternative splicing of hundreds of genes with functions of cell division, cellular senescence and transcription regulation. In addition, the changes in the expression level of miR-214-3p can cause changes in the alternative polyadenylation and 3UTR lengths of the transcript. Taken together, these results indicated that miR-214-3p could mediate apoptosis by diverse modes in AGS cells, which adds to the understanding of the critical role of miR-214-3p in cancer cancer.

2025-11-09 | GSE300926 | GEO

Gene expression profiling of MDA-MB-231 cells transfected with hsa-miR-205-5p and hsa-miR-214-3p compared to scrambled miRNA precursors

Project description:We have employed whole genome microarray to identify changes in gene expression in MDA-MB-231 cells transfected with hsa-miR-205-5p and hsa-miR-214-3p compared to scrambled miRNA precursors at 72 hours after transfection.

2020-05-31 | GSE148847 | GEO

T cell-derived miR-214 mediates perivascular fibrosis in hypertension

Project description:Despite increasing understanding of the prognostic importance of vascular stiffening linked to perivascular fibrosis in hypertension, the molecular and cellular regulation of this process is poorly understood. We aimed to study the functional role of microRNA-214 (miR-214) in the induction of perivascular fibrosis and endothelial dysfunction driving vascular stiffening. Out of 381 miRs screened in the perivascular tissues (PVAT) in response to angiotensin II (Ang II)-mediated hypertension, miR-214 showed the highest induction (8-fold, p<0.01). MiR-214 induction was pronounced in perivascular and circulating T cells, but not in PVAT adipocytes. Global deletion of miR-214-/- prevented Ang II-induced periaortic fibrosis Col1a1, Col3a1, Col5a1 and Tgfb1 expression, hydroxyproline accumulation and vascular stiffening, without difference in blood pressure. Mechanistic studies revealed that miR-214-/- mice were protected against endothelial dysfunction, oxidative stress and increased Nox2, all of which were induced by Ang II in WT mice. Ang II-induced recruitment of T cells into PVAT was abolished in miR-214-/- mice. Adoptive transfer of miR-214-/- T cells into RAG1-/- mice resulted in reduced perivascular fibrosis compared to the effect of WT T cells. Ang II induced hypertension caused significant change in the expression of 1380 T cell genes in WT, but only 51 in miR-214-/-. T cell activation, proliferation and chemotaxis pathways were differentially affected. miR-214-/- prevented Ang II-induction of pro-fibrotic T cell cytokines (IL-17, TNF, IL-9 and IFN) and chemokine receptors (CCR1, CCR2, CCR4, CCR5, CCR6 and CXCR3). This manifested in reduced in vitro and in vivo T cell chemotaxis resulting in attenuation of profibrotic perivascular inflammation. Translationally, we show that miR-214 is increased in plasma of hypertensive patients and is directly correlated to pulse wave velocity as a measure of vascular stiffness.

2020-02-29 | GSE143809 | GEO

Osteoclast-derived exosomal miR-214-3p inhibits osteoblastic bone formation.

Project description:Emerging evidence indicates that osteoclasts direct osteoblastic bone formation. MicroRNAs (miRNAs) have a crucial role in regulating osteoclast and osteoblast function. However, whether miRNAs mediate osteoclast-directed osteoblastic bone formation is mostly unknown. Here, we show that increased osteoclastic miR-214-3p associates with both elevated serum exosomal miR-214-3p and reduced bone formation in elderly women with fractures and in ovariectomized (OVX) mice. Osteoclast-specific miR-214-3p knock-in mice have elevated serum exosomal miR-214-3p and reduced bone formation that is rescued by osteoclast-targeted antagomir-214-3p treatment. We further demonstrate that osteoclast-derived exosomal miR-214-3p is transferred to osteoblasts to inhibit osteoblast activity in vitro and reduce bone formation in vivo. Moreover, osteoclast-targeted miR-214-3p inhibition promotes bone formation in ageing OVX mice. Collectively, our results suggest that osteoclast-derived exosomal miR-214-3p transfers to osteoblasts to inhibit bone formation. Inhibition of miR-214-3p in osteoclasts may be a strategy for treating skeletal disorders involving a reduction in bone formation.

| S-EPMC4786676 | biostudies-literature

Effect of miR-214-3p knockdown on global gene expression in prostate cancer cells

Project description:We analyzed the effect of knockdown of miR-214 compared to wild type on the expression of genes and pathways involved in prostate cancer cells.

2021-12-31 | E-MTAB-10782 | biostudies-arrayexpress

RNA-Seq analysis miR-455-3p overexpression effect on breast cancer cell line

Project description:MiR-455-3p has been reported to suppress the expression of ROCK2, HOXB5, hTERT, and RUNX2, which are involved in multiple biological processes including renal fibrosis, chondrogenic development and differentiation, Alzheimer’s disease, preeclampsia, and tumorigenesis. Here, we showed that miR-455-3p broadly inhibited TGF-beta-induced EMT by repressing the expression of Smad2, ZEB1, and HDAC2 in breast cancer cells, and that miR-455-3p loss-of-function promotes the acquisition of cell invasive properties and the ability to metastasize. These results indicate that miR-455-3p represents an important node that inhibits metastasis of breast cancer.

2019-09-06 | GSE129146 | GEO

Low miR-214-5p expression correlates with aggressive subtypes of pediatric ALCL with non-common histology

Project description:The small RNA landscape of pediatric ALK-positive ALCL was defined by RNA sequencing. Overall, 121 miRNAs were significantly dysregulated in ALCL compared to non-neoplastic lymph nodes. The most up-regulated miRNA was miR-21-5p, while miR-19a-3p and miR-214-5p were reduced in ALCL. Characterization of miRNA expression in cases that relapsed after first line therapy disclosed a significant association between miR-214-5p down-regulation and aggressive non-common histology.

2021-05-12 | GSE171323 | GEO

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