Ontology highlight
ABSTRACT:
PROVIDER: PRJNA788264 | ENA |
REPOSITORIES: ENA
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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
Project description:Silenced LINC01963 enhanced the chemosensitivity of prostate cancer cells to docetaxel by sponging miR-216b-5p to inhibit TrkB protein level
| PRJNA787914 | ENA
Project description:In this study, we used miRNA sequencing to analyze and identify possible miRNAs that can be regulated by and UBE2CP3 in gastric cancer. The results showed that lncRNA UBE2CP3 overexpression decreased the expression of miR-138-5p. Due to miR-138-5p was able to target ITGA2 expression, and UBE2CP3 knockdown significantly downregulates ITGA2 expression, we speculated UBE2CP3 may positively regulate ITGA2 expression through sponging miR-138-5p in GC.
2021-05-03 | GSE163814 | GEO
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
Project description:The aim of this study was evaluate the transcriptome changes in the comparison between MCF7 cells with increased expression of PAR-4 and the control cells before and after docetaxel treatment . The results generated could be of particular interest for the understanding the action of PAR-4 in chemosensitivity, especially to increase the specificity and effectiveness of drug treatment and overcoming resistance to chemotherapy.
2017-05-04 | GSE81064 | GEO
Project description:The transition from dividing progenitors into post-mitotic motor neurons is orchestrated by a series of events mainly studied at the transcriptional level by analyzing the activity of specific programming transcription factors. In this work, we describe that a motor neuron-specific transcriptional unit, harboring a lncRNA (lncMN2-203) and two miRNAs (miR-325-3p and miR-384-5p), controls such transition at the post-transcriptional level. Through the use of in vitro differentiation of mESC and single-cell sequencing of CRISPR/Cas9 mutants, we demonstrate that lncMN2-203 affects motor neuron differentiation by sponging miR-466i-5p and up-regulating its targets; among them Onecut2, which is the upstream regulator of the MN-specific programming factor Islet-1. In synergy with lncMN2-203, instead the depletion of the co-transcribed miR-325-3p and miR-384-5p was found to mainly sustain proliferation-related factors. These findings indicate the functional relevance of the MN2 locus and contribute to elucidate additional layers of regulation controlling the specificity of motor neuron differentiation.
2021-11-16 | GSE174671 | GEO
Project description:Impaired angiogenesis characterized by the reduced proliferation of pulmonary endothelial cells leads to reduced capillary density in patients with bronchopulmonary dysplasia (BPD). In a mouse model of BPD, perinatal hyperoxic injury decreases the number of the recently identified lung capillary stem cells termed as general capillary (gCap) cells, along with the specific reduction of Ntrk2, which encodes for Tropomyosin receptor kinase B (TRKB) within this subpopulation. Herein, we determine whether TRKB signaling is required for perinatal gCap cell proliferation and further promoting pulmonary angiogenesis using the hyperoxia mouse BPD model. TRKB activation by BDNF treatment led to enhanced tube-forming ability of endothelial cells in vitro. In vivo treatment of mice with BDNF increased the proliferation of gCap cells and alleviated capillary loss caused by hyperoxic injury. Conversely, inhibition of TRKB signaling disrupted the tube formation of endothelial cells and exaggerated the vascular endothelial damage caused by hyperoxia. We further show that MAPK/ERK signaling might act downstream of TRKB to modulate pulmonary angiogenesis. These data indicate that TRKB signaling play a critical role in pulmonary angiogenesis upon perinatal lung injury, supporting the concept that TRKB activation might be a potential therapeutic for preserving endothelial cells for lung diseases associated with prematurity.
2024-09-15 | GSE276575 | GEO
Project description:Background: TrkB-T1 is a BDNF receptor lacking a tyrosine kinase domain that is highly expressed in astrocytes and regulates BDNF-evoked calcium transients. Previous studies indicate that downregulation of TrkB-T1 in frontal cortex may be involved in neurobiological processes underlying suicide. Methods: In a microarray screening study (N=8), we interrogated all known microRNA in the frontal cortex of suicide completers with low expression of TrkB-T1 and normal controls. These findings were validated and followed up in a larger sample of cases and controls (N=55) Functional analyses included microRNA silencing, microRNA overexpression and luciferase assays to investigate specificity and to validate interactions between differentially expressed microRNA and TrkB-T1 Results: microRNAs Hsa-miR-185* and Hsa-miR-491-3p were upregulated in suicide completers with low expression of TrkB.T1 (Pnominal: 9.10-5 and 1.8.10-4 respectively; FDR-corrected p=0.031). Bioinformatic analyses revealed five putative binding sites for the DiGeorge syndrome linked microRNA Hsa-miR-185*in the 3M-bM-^@M-^YUTR of TrkB-T1, but none for Hsa-miR-491-3P. The increase of Hsa-miR-185* in frontal cortex of suicide completers was validated then confirmed in a larger, randomly selected group of suicide completers, where an inverse correlation between Hsa-miR-185* and TrkB-T1 expression was observed ( R=-0.404; p=0.002). Silencing and overexpression studies performed in human cell lines confirmed the inverse relationship between hsa-mir-185* and trkB-T1 expression. Luciferase assays demonstrated that Hsa-miR-185* binds to sequences in the 3M-bM-^@M-^YUTR of TrkB-T1. Conclusion: These results suggest that an increase of Hsa-miR-185* expression levels regulates, at least in part, the TrkB-T1 decrease observed in the frontal cortex of suicide completers and further implicate the 3MB 22q11 region in psychopathology. The microarray analysis consists in to compare the microRNA profile of four suicide completers with low TrkB-T1 expression level and four controls. Each RNA extract was labeled with Hy3 and hybridyzed with a reference sample labeled with Hy5. The reference sample was a pool of the eight RNA samples
2012-06-01 | E-GEOD-34120 | biostudies-arrayexpress
Project description:Lung cancer is an intrinsically highly metastatic disease and the leading cause of cancer-related deaths worldwide. Although discovery of molecular aberrations in lung adenocarcinomas has led to development of effective targeted therapies, corresponding “drivers” in lung squamous carcinomas (LUSC) have not materialized. Extensive molecular profiling has revealed LUSC tumors have non-recurrent somatic mutations and are largely driven by copy number alterations. Because microRNAs (miRs) play increasingly important roles in regulating metastasis-relevant pathways, we evaluated whether miRs can regulate LUSC progression. By integrating bioinformatics of the Cancer Genome Atlas (TCGA) with novel, highly metastatic LUSC models, we found that miR-671-5p is a key inhibitor of LUSC metastasis. Surprisingly, miR-671-5p regulates LUSC metastasis by inhibiting a circular RNA (circRNA), CDR1as. Although the putative function of CDR1as is through miR-7 sponging, we found miR-671-5p more potently silences an axis of CDR1as and its anti-sense transcript, cerebellar degeneration related antigen 1 (CDR1). To our knowledge, no function of CDR1 has ever been described. We found loss of CDR1as and CDR1 significantly inhibited LUSC metastases. Intriguingly, CDR1 was strongly associated with an epithelial-mesenchymal transition (EMT) program in LUSC tumors, and was sufficient to promote metastases, increased migration and substrate-independent survival, known as anoikis-resistance. CDR1, which directly interacts with AP1 and COPI subunits, no longer promoted migration and anoikis-resistance upon blockade of Golgi trafficking. Our findings reveal a miR/circRNA axis that regulates LUSC metastases through an enigmatic protein, CDR1.
2021-09-08 | PXD012286 | Pride
Project description:CircSry regulates spermatogenesis by enhancing γH2AX expression via sponging miR138-5p
| PRJNA767879 | ENA