MicroRNA-101-3p Modulates Mitochondrial Metabolism via the Regulation of Complex II Assembly
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA747895 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15186038.fastq.gz | Fastqsanger.gz | |||
| SRR15186039.fastq.gz | Fastqsanger.gz | |||
| SRR15186040.fastq.gz | Fastqsanger.gz | |||
| SRR15186041.fastq.gz | Fastqsanger.gz | |||
| SRR15186042.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
Similar Datasets
Project description:MicroRNA-101 (miR-101) is a tumour suppressor that regulates cancer proliferation and apoptotic signalling. Loss of miR-101 increases the expression of the Polycomb Repressive Complex 2 (PRC2) subunit enhancer of zeste homolog 2 (EZH2), resulting in alterations to the epigenome and enhanced tumorigenesis. MiR-101 has also been shown to modulate various aspects of cellular metabolism, however little is known about the mechanisms involved. To investigate the metabolic pathways that are regulated by miR-101, we performed transcriptome and functional analyses of osteosarcoma cells overexpressing miR-101. We found that miR-101 downregulates multiple mitochondrial processes, including oxidative phosphorylation, pyruvate metabolism, the citric acid cycle and phospholipid metabolism. We also found that miR-101 overexpression disrupts the transcription of mitochondrial DNA (mtDNA) via the downregulation of the mitochondrial transcription initiation complex proteins TFB2M and Mic60. These alterations in protein expression disrupt mitochondrial function, with significant decreases in both basal (54%) and maximal (67%) mitochondrial respiration rates. Native gel electrophoresis revealed that this diminished respiratory capacity was associated with reduced steady-state levels of mature succinate dehydrogenase (complex II), with a corresponding reduction of complex II enzymatic activity. Furthermore, miR-101 overexpression reduced the expression of the SDHB subunit, with a concomitant disruption of the assembly of the SDHC subunit into mature complex II. Overall, we describe a new role for miR-101 as a modulator of mitochondrial metabolism via its regulation of multiple mitochondrial processes, including mtDNA transcription and complex II biogenesis.
2021-07-20 | GSE180331 | GEO
Project description:Src modulates its oncogenic signaling via regulation of miRNA-129-3p [microRNA]
| PRJNA498643 | ENA
Project description:microRNA 27b-3p modulates SYK in Pediatric Asthma Induced by Dust Mites
| PRJNA491839 | ENA
Project description:SPRY4-IT1 (SPRY4 intronic transcript 1) is a long non-coding RNA (lncRNA) that was identified as a novel oncogene in various human cancers, including glioma. However, its function and the further mechanism in glioma remain largely unclear. Here, we aimed to investigate the role of SPRY4-IT1 in the development of glioma and its underlying molecular mechanism. We identify that SPRY4-IT1 is overexpressed in patients with glioma from the TCGA database and own cohort, and correlated with poor prognosis of patients. Then, loss of function and gain of function cell model were established by transfected with siRNA and pcDNA3.1 plasmid. SPRY4-IT1 promotes glioma cells proliferation by Cell Count Kit 8 assays and EdU assay in vitro, and xenograft tumor assays in vivo. RNA sequence was performed to compare the transcriptomes of U87 siSPRY4-IT1-NC and U87 siSPRY4-IT1 cells, and Gene Ontology (GO) enrichment analysis indicated angiogenesis is significantly enriched. HUVEC tube forming assays and Chick Embryo Chorioallantoic Membrane (CAM) assays confirmed that SPRY4-IT1 can induce angiogenesis of glioma in vitro and in vivo. Mechanistically, we identify that SPRY4-IT1 upregulates EZH2 expression by sponge miR-101-3p to induce VEGFA expression in glioma cells. Moreover, SPRY4-IT1 activates VEGFR2/AKT/ERK1/2 pathway in HUVECs by glioma cell-mediated. Rescue experiments were performed by co-transfected with SPRY4-IT1 and EZH2 overexpression plasmid in glioma cells, and confirmed that SPRY4-IT1 promotes cell proliferation and angiogenesis of glioma by miR-101-3p/EZH2/VEGFA signaling axis. Taken together, our studies clarify that SPRY4-IT1 upregulates EZH2 to induce VEGFA by sponge miR-101-3p to achieve cell proliferation and angiogenesis in glioma. Thus, these findings have provided insights into the prognosis prediction and therapeutic target of glioma.
2022-06-30 | GSE189462 | GEO
Project description:To determine the phenotypic overlap between restoring miR-101 expression in bladder cancer cells and knocking down EZH2. Either control precursors, pre-miR-101, control siRNA, or EZH2 siRNA were transfected in triplicate into UM-UC-3 cells for 72 hours at a final concentration of 50 nM.
2010-06-25 | E-GEOD-13674 | biostudies-arrayexpress
Project description:To determine the phenotypic overlap between restoring miR-101 expression in bladder cancer cells and knocking down EZH2.
2009-03-11 | GSE13674 | GEO
Project description:According to our previous discovery that miR-552-3p could regulate the gene expression both in cytoplasm and nucleus. Furthermore, we found the sequence in miR-552-3p was similar with cis-elements of NR1 subfamily, the important regulator of glycolipid metabolism, suggesting miR-552-3p may play a pivotal role in metabolism. To find the genes regulated by miR-5523-p, RNA-seq was used and the difference expression genes in HepG2 cells transfected with miR-552-3p or negative control was detected. Meanwhile, to found which genes are regulated by cytoplasmic miR-552-3p or nuclear miR-552-3p, importin8 expression was silenced by siRNA in the HepG2 cell and the effect of miR-552-3p on the genes expression was detected. The results of this study are showed the genes regulated by miR-552-3p and distinguish which genes are regulated by the cytoplasmic miR-552-3p or nuclear miR-552-3p.
2020-07-15 | GSE154384 | GEO
Project description:Primary cilium serves as a cellular M-bM-^@M-^\antennaM-bM-^@M-^] to sense environmental signals. Ciliogenesis requires the removal of CP110 to convert the mother centriole into the basal body. Actin dynamics is also critical for cilia formation. How these distinct processes are properly regulated remains unknown. Here we show that miR-129-3p, a microRNA conserved in the vertebrates, controlled cilia assembly by down-regulating both CP110 and four proteins critical for actin dynamics, Arp2, Toca1, abLIM1, and abLIM3. Consistently, blocking miR-129-3p repressed cilia formation in cultured mammalian cells, whereas its overexpression potently induced ciliogenesis in proliferating cells and extraordinary cilia elongation. Moreover, inhibition of miR-129-3p in zebrafish embryos suppressed cilia assembly in the KupfferM-bM-^@M-^Ys vesicle and pronephric duct, leading to developmental abnormalities including curved body, pericardial oedema, and randomised left-right patterning. Our results thus unravel a novel mechanism that orchestrates both the centriole-to-basal body transition and subsequent cilia assembly via microRNA-mediated posttranscriptional regulations. We want to find the targets of miR-129-3p by overexpressing miR-129-3p oligo or control oligo in hTERT-RPE1 cells. Through microarray analysis we could check the downregulated genes and these genes might be the targets of miR-129-3p. RPE1 cells were transfected with control (Ctrl) or miR-129-3p (M129) oligo for 72h, and harvested for RNA extraction and hybridization on Affymetrix microarrays. Two samples: RPE1-Ctrl, RPE1-M129
2012-05-31 | E-GEOD-34846 | biostudies-arrayexpress
Project description:Autotaxin (ATX), a vital enzyme that generates lysophosphatidic acid (LPA), affects many biological processes, including tumorigenesis, via the ATX-LPA axis. In this study, we demonstrate that microRNA-101-3p (miR-101-3p), a well-known tumor suppressor, downregulates ATX expression at the posttranscriptional level. We found that miR-101-3p inhibits ATX regulation by directly targeting a conserved sequence in the ATX mRNA 3'UTR. Moreover, we observed an inverse correlation between ATX and miR-101-3p levels in various types of cancer cells. ATX is highly expressed in several human cancers. Here, we verified that ATX expression is significantly inhibited by miR-101-3p in U87 and HCT116 cells. ATX downregulation contributed to the suppression of migration, invasion, and proliferation mediated by miR-101-3p; furthermore, the tumor-suppressing activity of miR-101-3p was partially reduced by the addition of LPA in U87 cells. Our data suggest that ATX is a novel target of miR-101-3p.
| S-EPMC6443858 | biostudies-literature
Project description:Src modulates its oncogenic signaling via regulation of miRNA-129-3p
| PRJNA498642 | ENA