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Mir-383-5P Regulated By The Transcription Factor Ctcf

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We found that CTCF inhibited miR-383-5p expression via its enrichment in the promoter region of miR-383-5p, whereas the miR-383-5p targeted and inhibited HDAC9 expression. We found that CTCF inhibited miR-383-5p expression via its enrichment in the promoter region of miR-383-5p, whereas the miR-383-5p targeted and inhibited HDAC9 expression.

During the osteogenic differentiation of hPDLSCs, miR-383-5p expression was gradually up-regulated, while HDAC9 mRNA level was down-regulated. HDAC9 overexpression suppressed Alkaline phosphatase activity, mineral node formation and the expressions of osteogenic markers including Runx family transcription factor 2 (RUNX2), osteocalcin and A master regulatory protein transcription factors involved in called CCCTC-binding factor (CTCF) helps bridge the gap between genome architecture and gene expression. A wide range of CTCF-binding sites are dotted throughout the The down-regulation of miR-383-5p and up-regulation of PD-L1 in breast cancer tissues and cell lines The expression level of miR-383-5p and PD-L1 were measured in 24 pairs of clinical samples.

The roles of E2F7 in cancer: Current knowledge and future prospects

Effects of the miR-383-5p expression level on proliferation 48 h after ...

Up-regulation of miR-383 knocks down the expression of PRDX3, inhibits cell proliferation and promotes apoptosis. Expression of hsa-miR-373 miR 383 as is down-regulated by aberrant methylation in colon cancer and that this miRNA may function by regulating expression of

Moreover, here we elucidated the mechanism through which TRF2 exerts its activity as a transcriptional regulator of miRNA expression. We showed that the control of miR-193b-3p expression is mediated by the coordinated activity of TRF2 with CTCF, a chromatin organization factor that modulates gene expression.

Transcription, a first step of gene expression, is regulated by transcription factors, RNA polymerases, and chromatin modifying proteins. The E2F is a family of transcription factors involved in various cellular model of MCAO processes. Three replicates were performed. from publication: miR-383-5p Regulated by the Transcription Factor CTCF Affects Neuronal Impairment in Cerebral Ischemia by Mediating Deacetylase HDAC9 Activity

^ Shen J, Han Q, Li W, Chen X, Lu J, Zheng J, Xue S (August 2022). „miR-383-5p Regulated by the Transcription Factor CTCF Affects Neuronal Impairment in Cerebral Ischemia by Mediating Deacetylase HDAC9 Activity“. In gliomas, miR-383 targets insulin-like growth factor 1 receptor (IGF1R), leading to suppression of AKT signaling and downregulation and chromatin modifying proteins of matrix metalloproteinase 2 (MMP2), thereby inhibiting glioma cell invasion. Its downregulation correlates with higher pathological grades in gliomas (He et al. 2013). We found that CTCF inhibited miR-383-5p expression via its enrichment in the promoter region of miR-383-5p, whereas the miR-383-5p targeted and inhibited HDAC9 expression.

  • The effect of miR-383 on neurological scores after MCAO
  • The roles of miR-383 as a diagnostic and prognostic
  • The expression of miR-383 both in MCAO and injection

Results miR-383 was down-regulated significantly in tumor tissues, while IL-17 was up-regulated. IL-17 was certificated to act as the downstream gene of miR-383. Furthermore, overexpression of miR-383 suppressed cell proliferation and promoted apoptosis in Download scientific diagram | MiR-383 regulates the expression of PPARγ in vivo. Overexpression of miR-383 by miR-383 agomir injection downregulated PPARγ protein level 24h after MCAO. As shown by the graphical abstract, we first showed that PCGEM1 was up-regulated in CRC cells and was activated by transcription factor CTCF. Knockdown either CTCF or PCGEM1 could decrease CRC cell proliferation and migration while inducing cell apoptosis.

Prostate cancer gene expression marker 1 (PCGEM1) has been identified as an oncogenic long non-coding RNA (lncRNA) in diverse cancers, but it has never been linked with colorectal cancer (CRC). Former studies have shown the mutual regulation between lncRNAs and transcription factors (TFs) in cancer. CCCTC binding factor (CTCF) has been reported to 中风是全球长期残疾的主要原因，是由脑动脉 阻塞或出血引起的。由此产生的脑缺血导致局部神经元死亡和脑损伤。据报道，组蛋白去乙酰化酶 9 (HDAC9) 在缺血性脑损伤中升高，但其在中风中的机制仍然是个谜。本研究旨在揭示HDAC9表达的调控方式以及HDAC9激活对脑缺血神经元功能的影响。利用生物 Transcriptional repressor CTCF also known as 11-zinc finger protein or CCCTC-binding factor is a transcription factor that in humans is encoded by the CTCF gene. [5][6] CTCF is involved in many cellular processes, including transcriptional regulation, insulator activity, V (D)J recombination [7] and regulation of chromatin architecture.

We found that miR-383-5p is downregulated in retinal ganglion cells in response to zymosan-induced intraocular inflammation. MiR-383-5p downregulation in neurons is sufficient to promote axon growth in vitro, and the intravitreal injection of a miR-383-5p inhibitor into the eye promotes axon regeneration following optic nerve crush. Equol an isoflavonoid: potential for improved prostate health, in vitro and in vivoevidence Integration interactions between regulatory analysis of microRNA and mRNA paired expression profiling identifies deregulated microRNA-transcription factor-gene regulatory networks in ovarian endometriosis Selection of gonadotrophin surge attenuating factor phage antibodies by bioassay Download scientific diagram | The effect of miR-383 on neurological scores after MCAO. The evaluation indexes were as following: (1) spontaneous Activity; (2) climbing; (3) forepaw outstretching

Download scientific diagram | The expression of miR-383 both in MCAO and injection rats. (A) Decrease in miR-383 in a rat model of MCAO after 24h surgery. * P < 0.05 vs sham, n=3 in each group. (B

We found that CTCF inhibited miR-383-5p expression via its enrichment in the promoter region of miR-383-5p, whereas the miR-383-5p targeted and inhibited HDAC9 expression. CTCF, chromatin loops and transcription regulation at selected gene loci. (a) Genes at the β-globin locus are under control of the locus control region (LCR). CTCF-binding sites interact to create a chromatin hub with a loop encompassing the LCR and the β-globin genes. Upon erythroid differentiation, erythroid-specific transcription factors and cohesin enable the For example, Jiang et al found that miR-383-5p reduced ovarian cancer cells proliferation and enhanced chemo-sensitivity via regulating TRIM27 expression. 24 Wang et al showed that AKR1B10 modulated regulated by miR-383-5p, promoted HCC progression. 25 However, the roles of miR-383-5p in TNBC remain unclear.

  • MicroRNA-383: A tumor suppressor miRNA in human cancer
  • The roles of E2F7 in cancer: Current knowledge and future prospects
  • CCCTC-binding factor-mediated microRNA-340-5p suppression
  • Role of CTCF in the regulation of microRNA expression
  • Transcription Factor CTCF

During the osteogenic differentiation of hPDLSCs, miR-383-5p expression was gradually up-regulated, while HDAC9 mRNA level was down-regulated. HDAC9 overexpression suppressed Alkaline phosphatase activity, mineral node formation and the expressions of osteogenic markers including Runx family transcription factor 2 (RUNX2), osteocalcin and Strikingly, we also discovered that miR-483 enhances its own transcription by up-regulation of the transcription factor USF1, which activates a promoter element upstream of the MIR483 gene. However, since the USF1 mRNA lacks binding sites for miR-483-5p and -3p, USF1 expression is likely enhanced in an indirect manner. This suggests multiple ways in which CTCF may impact gene expression. At promoters, CTCF can directly affect transcription. At more distal sites, CTCF may orchestrate interactions between regulatory elements and help separate eu‐ and heterochromatic areas in the genome, exerting a chromatin barrier function.

Furthermore, patients with low miR-383-5p expression levels had a significantly decreased overall survival and disease-free survival rate compared with those with high miR-383-5p expression levels (Fig. 1A and B). Table I. Clinical association of miR-383-5p expression in lung adenocarcinoma. Abstract. Vascular endothelial cell functions afect lower extremity arteriosclerosis obliterans (LEASO), while alpha-2-macroglobulin (A2M) and CCCTC-binding factor (CTCF) are closely related to the function of such cells. This paper aims to identify the inluences of CTCF on vas-cular endothelial cells in LEASO by regulating A2M. A rat model of LEASO was established to Complete information for MIR383 gene (RNA Gene), MicroRNA 383, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards – The Human Gene Compendium

Inhibition of miR-383 by miR-383 antagomir significantly reduces infarct size in the rats of MCAO. The x-axis represents the anterior to posterior distance from the bregma.

GeneRIFs: Gene References Into Functions The novel circFKBP8/miR-432-5p/E2F7 cascade functions as a regulatory network in breast cancer. Transcription Factor E2F7 Hampers the Killing Effect of NK Cells against Colorectal Cancer Cells via Activating RAD18 Transcription. p53/E2F7 axis promotes temozolomide chemoresistance in glioblastoma

In addition, up-regulation of miR-383-5p decreased the IC50 value of ovarian cancer cells to paclitaxel and increased cell apoptosis rate under the treatment of paclitaxel, indicating that overexpressed miR-383-5p enhanced chemosensitivity in ovarian cancer cells. The miR-383 was initially found as a tumor suppressor and prognostic marker in different human cancers. The regulation of miR-383 and its target gene expression could be helpful in the prevention of tumorigenesis, improving cancer prognosis, and enhancing 5-year survival of patients with cancer.

Functional role of hub molecules in miRNA and transcription factor mediated gene regulatory network of colorectal and lung cancer Therefore, during induced transdifferentiation, the transcription factor can directly reorganize the 3D chromatin interactions, and perturbation of CTCF-mediated genome topology may resolve the limitations of cell fate transitions.