Similar Datasets
Project description:ATAC-seq was performed to identify the cis-regulatory genomic elements in in primary human naïve and memory T cells untreated or activated with anti-CD3 and anti-CD28 antibodies for one or three days.
2022-01-10 | GSE161096 | GEO
Project description:Within the immune system, microRNAs (miRNAs) exert key regulatory functions. However, what are the mRNA targets regulated by miRNAs and how miRNAs are transcriptionally regulated themselves remain for the most part unknown. We found that in primary human memory T helper lymphocytes, miR-150 was the most abundantly expressed miRNA, and its expression decreased drastically upon activation, suggesting regulatory roles. Constitutive MIR150 gene expression required the RFX family of transcription factors, and its activation-induced down-regulation was linked to their reduced expression. By performing miRNA pull-down and sequencing experiments, we identified PDGFA-associated protein 1 (PDAP1) as one main target of miR-150 in human T lymphocytes. PDAP1 acted as an RNA-binding protein (RBP), and its CRISPR/Cas-9-mediated deletion revealed that it prominently contributed to the regulation of T-cell proliferation. Overall, using an integrated approach involving quantitative analysis, unbiased genomics, and genome editing, we identified RFX factors, miR-150, and the PDAP1 RBP as the components of a regulatory axis that restrains proliferation of primary human T lymphocytes.
| S-EPMC8865640 | biostudies-literature
Project description:An RFX/miR-150 axis restrains proliferation of primary human T lymphocytes
| PRJNA675555 | ENA
Project description:An RFX/miR-150 axis regulates proliferation of primary human T lymphocytes
| PRJNA675570 | ENA
Project description:The aberrant expansion of B1a cells has been observed in several murine autoimmune disease models; however, the mechanism of such proliferation of B1a cells is still limited. Here, we identify that Myb Like, SWIRM And MPN Domains 1 (MYSM1), a histone H2A deubiquitinase, plays an intrinsic role in the proliferation of B1a cells where MYSM1 deficiency results in the increased proliferation of B1a cells in mice. We demonstrate that MYSM1 recruits c-Myc to the promoter of miR-150 and stimulates the transcription of miR-150. Our further investigation shows that miR-150 decreases FMS-like tyrosine kinase 3 (FLT3) in B1a cells. In agreement with our animal studies, the percentage of FLT3+ B1 cells in Systemic Lupus Erythematosus (SLE) patients is significantly higher than healthy control. Thus, this study uncovers a novel pathway MYSM1/miR-150/FLT3 that inhibits proliferation of B1a, which may be involved in the pathogenesis of SLE.
| S-EPMC5356540 | biostudies-literature
Project description:MicroRNAs (miRNAs), a class of small non-coding linear RNAs, have been shown to play a crucial role in erythropoiesis. To evaluate the indispensable role of constant suppression of miR-150 during terminal erythropoiesis, we performed miR-150 gain- and loss-of-function experiments on hemin-induced K562 cells and EPO-induced human CD34+ cells. We found that forced expression of miR-150 suppresses commitment of hemoglobinization and CD235a labeling in both cell types. Erythroid proliferation is also inhibited via inducing apoptosis and blocking the cell cycle when miR-150 is overexpressed. In contrast, miR-150 inhibition promotes terminal erythropoiesis. 4.1 R gene is a new target of miR-150 during terminal erythropoiesis, and its abundance ensures the mechanical stability and deformability of the membrane. However, knockdown of 4.1 R did not affect terminal erythropoiesis. Transcriptional profiling identified more molecules involved in terminal erythroid dysregulation derived from miR-150 overexpression. These results shed light on the role of miR-150 during human terminal erythropoiesis. This is the first report highlighting the relationship between miRNA and membrane protein and enhancing our understanding of how miRNA works in the hematopoietic system.
| S-EPMC4767489 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2017-01-01 | GSE87590 | GEO
Project description:Long noncoding RNA (lncRNA) MAF BZIP transcription factor G antisense RNA 1 (MAFG‑AS1) has been demonstrated to serve an important role in the progression of various types of cancer, whereas its role in breast cancer has not been fully elucidated. The present study aimed to explore the potential role and underlying mechanism of MAFG‑AS1 in breast cancer. To achieve this, the expression of MAFG‑AS1, microRNA (miR)‑150‑5p and MYB was detected by reverse transcription‑quantitative PCR. The binding between miR‑150‑5p and MAFG‑AS1 or MYB was verified using a luciferase reporter assay. Cell proliferation was analyzed by MTS, apoptosis and cell cycle were detected by Annexin V/propidium iodide, and cell migration was analyzed by wound healing assay. The results demonstrated that the expression levels of MAFG‑AS1 were significantly upregulated in breast cancer tissues and cells compared with those in normal breast tissues and cells. High MAFG‑AS1 expression promoted the proliferation, migration and epithelial‑mesenchymal transition of breast cancer cells. By contrast, miR‑150‑5p expression was reduced in breast cancer tissues compared with that in healthy breast tissues, and low expression of miR‑150‑5p was associated with poor overall survival in patients with breast cancer. Bioinformatics and luciferase assay revealed that MAFG‑AS1 served as a sponge of miR‑150‑5p, and that miR‑150‑5p bound to MYB. The functional rescue assay results demonstrated that MAFG‑AS1 knockdown suppressed the proliferation and migration of breast cancer cells by regulating miR‑150‑5p, which in turn targeted MYB. In conclusion, the results of the present study demonstrated that MAFG‑AS1 functioned as a novel oncogenic lncRNA in the development of human breast cancer via regulating the miR‑150‑5p/MYB axis, which suggested that MAFG‑AS1 may be a novel biomarker for the diagnosis and prognosis of human breast cancer.
| S-EPMC7721084 | biostudies-literature
Project description:Circular RNA 0000511 (circ_0000511) has been observed to be dysregulated in breast cancer (BC). However, the functions of circ_0000511 in breast cancer remain unknown. The expression levels of circ_0000511, ribonuclease P RNA component H1, microRNA‑326 (miR‑326) and transcriptional co‑activator with PDZ‑binding motif (TAZ) were examined by reverse transcription‑quantitative PCR. Colony formation and MTT assays were conducted to analyze the cellular proliferative ability. The apoptotic rate was assessed by flow cytometry. Western blot analysis was used to evaluate the expression levels of B cell leukemia/lymphoma 2 (Bcl‑2), Bcl‑2 associated X apoptosis regulator, cleaved caspase‑3 and TAZ. Transwell assays were performed to evaluate the migration and invasion of BC cells. The target interaction between miR‑326 and circ_0000511 or TAZ was confirmed by dual‑luciferase reporter assay. Xenograft assay was used to identify the function of circ_0000511 in vivo. Circ_0000511 abundance was abnormally elevated in BC tissue samples and cell lines compared with in matched normal cases. Circ_0000511 interference suppressed the proliferation, migration and invasion, and induced apoptosis of BC cells. miR‑326 was a direct target of circ_0000511, and circ_0000511 silencing‑mediated effects in BC cells were largely reversed by the knockdown of miR‑326. miR‑326 directly bound to TAZ mRNA, and TAZ accumulation largely attenuated miR‑326 overexpression‑induced effects in BC cells. Circ_0000511 upregulated the expression levels of TAZ partly via targeting miR‑326 in BC cells. Circ_0000511 silencing restrained tumor growth in vivo. Circ_0000511 accelerated the proliferation, migration and invasion, while inhibiting the apoptosis of BC cells through upregulating TAZ expression via sponging miR‑326. The circ_0000511/miR‑326/TAZ axis may be a novel therapeutic target for BC treatment.
| S-EPMC7891826 | biostudies-literature
Project description:BackgroundTo characterize the MIAT expression in cervical cancer and elucidate its mechanistic involvement in the tumor biology of this disease.MethodsThe relative expression of MIAT and miR-150 was determined by real-time PCR. Cell proliferation was measured by the CCK-8 and clonogenic assay. The anchorage-independent growth was evaluated by soft agar assay. The in vivo tumor progression was assayed with xenograft mice model. The regulatory effect of miR-150 on MIAT was interrogated by luciferase reporter assay. The endogenous CNKD1B protein was detected by western blotting.ResultsThe low expression of MIAT was characterized in cervical cancer, which associated with relatively poor prognosis. Ectopic expression of MIAT inhibited malignant growth of cervical cancer both in vitro and in vivo. Mechanistically, MIAT regulated CDKN1B expression via competition with miR-150, and miR-150-inhibition directly suppressed cervical cancer cell growth.ConclusionsOur study characterized the anti-tumor property of MIAT in cervical cancer and elucidated its competitively regulation of CDKN1B with miR-150. Our data highlighted the critical role of MIAT-miR-150-CDKN1B signaling axis in cervical cancer.
| S-EPMC7296772 | biostudies-literature