The Role of Long Non-coding RNA, Nuclear Enriched Abundant Transcript 1 (NEAT1) in Cancer and Other Pathologies

2021 ◽  
Author(s):  
Miao Zhang ◽  
Jianmin Guo ◽  
Lifei Liu ◽  
Mei Huang ◽  
Yuexuan Li ◽  
...  
Keyword(s):  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Abundant Transcript

scholarly journals Long non-coding RNA NEAT1 deteriorates polycystic ovary syndrome progression via binding microRNA-324-3p to target bromodomain containing 3

2021 ◽  
Author(s):  
Le Wu ◽  
zhijian Tu ◽  
bao Ying ◽  
Zhai Qi ◽  
lixu Jin
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Metabolic Disorders ◽  
Regulatory Mechanism ◽  
Polycystic Ovary ◽  
Ovary Syndrome ◽  
Non Coding Rna ◽  
Biochemical Indices ◽  
Long Non Coding Rna ◽  
Abundant Transcript

Abstract Objective: Long non-coding RNA (LncRNA) nuclear-enriched abundant transcript 1 (NEAT1) has been studied in polycystic ovary syndrome (PCOS), while the regulatory mechanism of NEAT1 on PCOS by regulating microRNA (miR)-324-3p remains extensive exploration. Our study aims to investigate the role of NEAT1, miR-324-3p and bromodomain containing 3 (BRD3) in PCOS.Methods: Firstly, the PCOS rat model was established, and then NEAT1, miR-324-3p and BRD3 levels were detected in PCOS rats. The decreased NEAT1 or augmented miR-324-3p were injected into the PCOS rats to determine the change of biochemical indices and pathology. Also, the rescue experiment was conducted. Thereafter, the binding relations among NEAT1, miR-324-3p and BRD3 were analyzed.Results: NEAT1 and BRD3 were enriched while miR-324-3p was decreased in PCOS rats. The reduction of NEAT1 or the elevation of miR-324-3p mitigated the obesity and metabolic disorders in PCOS rats. NEAT1 sponged miR-324-3p as a competing endogenous RNA and miR-324-3p targeted BRD3. The elevated miR-324-3p or reduced BRD3 reversed effects of enhanced NEAT1.Conclusion: NEAT1 exacerbates obesity and metabolic disorders of PCOS rats via regulating miR-324-3p to target BRD3. This study affords a novel direction for PCOS treatment.

scholarly journals The Implications of the Long Non-Coding RNA NEAT1 in Non-Cancerous Diseases

2019 ◽  
Vol 20 (3) ◽  
pp. 627 ◽  
Author(s):  
Felix Prinz ◽  
Anita Kapeller ◽  
Martin Pichler ◽  
Christiane Klec
Keyword(s):  
Viral Infections ◽  
Special Focus ◽  
Nuclear Retention ◽  
Cellular Processes ◽  
Mediated Effects ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Transcriptional Induction ◽  
Abundant Transcript

Long non-coding RNAs (lncRNAs) are involved in a variety of biological and cellular processes as well as in physiologic and pathophysiologic events. This review summarizes recent literature about the role of the lncRNA nuclear enriched abundant transcript 1 (NEAT1) in non-cancerous diseases with a special focus on viral infections and neurodegenerative diseases. In contrast to its role as competing endogenous RNA (ceRNA) in carcinogenesis, NEAT1’s function in non-cancerous diseases predominantly focuses on paraspeckle-mediated effects on gene expression. This involves processes such as nuclear retention of mRNAs or sequestration of paraspeckle proteins from specific promoters, resulting in transcriptional induction or repression of genes involved in regulating the immune system or neurodegenerative processes. NEAT1 expression is aberrantly—mostly upregulated—in non-cancerous pathological conditions, indicating that it could serve as potential prognostic biomarker. Additional studies are needed to elucidate NEAT1’s capability to be a therapeutic target for non-cancerous diseases.

scholarly journals Role of Long Non-Coding RNA Polymorphisms in Cancer Chemotherapeutic Response

2021 ◽  
Vol 11 (6) ◽  
pp. 513
Author(s):  
Zheng Zhang ◽  
Meng Gu ◽  
Zhongze Gu ◽  
Yan-Ru Lou
Keyword(s):  
Molecular Mechanisms ◽  
Neurological Diseases ◽  
Cellular Processes ◽  
Dna And Rna ◽  
Chemotherapeutic Response ◽  
Non Coding Rna ◽  
Response To Chemotherapy ◽  
Personalized Oncology ◽  
Long Non Coding Rna

Genetic polymorphisms are defined as the presence of two or more different alleles in the same locus, with a frequency higher than 1% in the population. Since the discovery of long non-coding RNAs (lncRNAs), which refer to a non-coding RNA with a length of more than 200 nucleotides, their biological roles have been increasingly revealed in recent years. They regulate many cellular processes, from pluripotency to cancer. Interestingly, abnormal expression or dysfunction of lncRNAs is closely related to the occurrence of human diseases, including cancer and degenerative neurological diseases. Particularly, their polymorphisms have been found to be associated with altered drug response and/or drug toxicity in cancer treatment. However, molecular mechanisms are not yet fully elucidated, which are expected to be discovered by detailed studies of RNA–protein, RNA–DNA, and RNA–lipid interactions. In conclusion, lncRNAs polymorphisms may become biomarkers for predicting the response to chemotherapy in cancer patients. Here we review and discuss how gene polymorphisms of lncRNAs affect cancer chemotherapeutic response. This knowledge may pave the way to personalized oncology treatments.

scholarly journals LncRNA PVT1 promotes cervical cancer progression by sponging miR-503 to upregulate ARL2 expression

2021 ◽  
Vol 16 (1) ◽  
pp. 1-13
Author(s):  
Weiwei Liu ◽  
Dongmei Yao ◽  
Bo Huang
Keyword(s):  
Cervical Cancer ◽  
Cancer Progression ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Nude Mouse Model ◽  
Western Blot Assay ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Cervical cancer (CC) is a huge threat to the health of women worldwide. Long non-coding RNA plasmacytoma variant translocation 1 gene (PVT1) was proved to be associated with the development of diverse human cancers, including CC. Nevertheless, the exact mechanism of PVT1 in CC progression remains unclear. Levels of PVT1, microRNA-503 (miR-503), and ADP ribosylation factor-like protein 2 (ARL2) were measured by quantitative reverse transcription-polymerase chain reaction or western blot assay. 3-(4,5)-Dimethylthiazole-2-y1)-2,5-biphenyl tetrazolium bromide (MTT) and flow cytometry were used to examine cell viability and apoptosis, respectively. For migration and invasion detection, transwell assay was performed. The interaction between miR-503 and PVT1 or ARL2 was shown by dual luciferase reporter assay. A nude mouse model was constructed to clarify the role of PVT1 in vivo. PVT1 and ARL2 expressions were increased, whereas miR-503 expression was decreased in CC tissues and cells. PVT1 was a sponge of miR-503, and miR-503 targeted ARL2. PVT1 knockdown suppressed proliferation, migration, and invasion of CC cells, which could be largely reverted by miR-503 inhibitor. In addition, upregulated ARL2 could attenuate si-PVT1-mediated anti-proliferation and anti-metastasis effects on CC cells. Silenced PVT1 also inhibited CC tumor growth in vivo. PVT1 knockdown exerted tumor suppressor role in CC progression via the miR-503/ARL2 axis, at least in part.

scholarly journals Long non-coding RNA LINC00665 promotes gemcitabine resistance of Cholangiocarcinoma cells via regulating EMT and stemness properties through miR-424-5p/BCL9L axis

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Min Lu ◽  
Xinglei Qin ◽  
Yajun Zhou ◽  
Gang Li ◽  
Zhaoyang Liu ◽  
...  
Keyword(s):  
Acquired Resistance ◽  
Transcriptional Regulators ◽  
First Line ◽  
Protein Coding ◽  
Gemcitabine Resistance ◽  
Non Coding Rna ◽  
Sphere Formation ◽  
Long Non Coding Rna ◽  
Line Chemotherapy

AbstractGemcitabine is the first-line chemotherapy drug for cholangiocarcinoma (CCA), but acquired resistance has been frequently observed in CCA patients. To search for potential long noncoding RNAs (lncRNAs) involved in gemcitabine resistance, two gemcitabine resistant CCA cell lines were established and dysregulated lncRNAs were identified by lncRNA microarray. Long intergenic non-protein coding RNA 665 (LINC00665) were found to rank the top 10 upregulated lncRNAs in our study, and high LINC00665 expression was closely associated with poor prognosis and chemoresistance of CCA patients. Silencing LINC00665 in gemcitabine resistant CCA cells impaired gemcitabine tolerance, while enforced LINC00665 expression increased gemcitabine resistance of sensitive CCA cells. The gemcitabine resistant CCA cells showed increased EMT and stemness properties, and silencing LINC00665 suppressed sphere formation, migration, invasion and expression of EMT and stemness markers. In addition, Wnt/β-Catenin signaling was activated in gemcitabine resistant CCA cells, but LINC00665 knockdown suppressed Wnt/β-Catenin activation. B-cell CLL/lymphoma 9-like (BCL9L), the nucleus transcriptional regulators of Wnt/β-Catenin signaling, plays a key role in the nucleus translocation of β-Catenin and promotes β-Catenin-dependent transcription. In our study, we found that LINC00665 regulated BCL9L expression by acting as a molecular sponge for miR-424-5p. Moreover, silencing BCL9L or miR-424-5p overexpression suppressed gemcitabine resistance, EMT, stemness and Wnt/β-Catenin activation in resistant CCA cells. In conclusion, our results disclosed the important role of LINC00665 in gemcitabine resistance of CCA cells, and provided a new biomarker or therapeutic target for CCA treament.

scholarly journals Role of long non-coding RNA-RNCR3 in atherosclerosis-related vascular dysfunction

2016 ◽  
Vol 7 (6) ◽  
pp. e2248-e2248 ◽  
Author(s):  
K Shan ◽  
Q Jiang ◽  
X -Q Wang ◽  
Y -N -Z Wang ◽  
H Yang ◽  
...  
Keyword(s):  
Vascular Dysfunction ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Role of the Long Non-Coding RNA MAPT-AS1 in Regulation of Microtubule Associated Protein Tau (MAPT) Expression in Parkinson's Disease

PLoS ONE ◽  
2016 ◽  
Vol 11 (6) ◽  
pp. e0157924 ◽  
Author(s):  
Kirsten G. Coupland ◽  
Woojin S. Kim ◽  
Glenda M. Halliday ◽  
Marianne Hallupp ◽  
Carol Dobson-Stone ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Protein Tau ◽  
Microtubule Associated Protein Tau ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract TMP25: Long Non-Coding RNA Mediates Stroke-Induced Neurogenesis

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Baoyan Fan ◽  
Wanlong Pan ◽  
Xinli Wang ◽  
Michael Chopp ◽  
Zheng Gang Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Regulation Of Gene Expression ◽  
Artery Occlusion ◽  
Loss Of Function ◽  
Bioinformatics Analyses ◽  
Guide Rna ◽  
Non Coding Rna ◽  
Cerebral Artery Occlusion ◽  
Long Non Coding Rna

Background and Purpose: Adult neurogenesis contributes to functional recovery after stroke. Long non-coding RNAs (lncRNAs) regulate stem cell self-renewal and differentiation. However, the role of lncRNAs in stroke-induced neurogenesis remains unknown. Methods and Results: Using lncRNA array and in situ hybridization, we analyzed lncRNA profiles of adult neural stem cells (NSCs) isolated from the subventricular zone neurogenic region in rats subjected to middle cerebral artery occlusion. We found that H19 was the most highly upregulated lncRNA (19 fold) in ischemic NSCs compared with non-ischemic NSCs. Reduction of endogenous H19 in NSCs by CRISPR-Cas9 genome editing significantly decreased the proliferation and increased the apoptosis of ischemic NSCs, as assayed by the number of BrdU + cells (56±5% vs 22±3%, p<0.01, n=3) and Caspase-3/7 activity compared to NSCs transfected with scrambled small guide RNA (sgRNA). Knockdown of H19 significantly decreased the number of Tuj1 + neuroblasts (8±2% vs 5±0.4%, p<0.01, n=3) and NG 2 + oliogodendrocyte progenitor cells (10±1% vs 5±0.3%, p<0.01, n=3), suggesting that deletion of H19 suppresses the proliferation and survival and blocks the differentiation of NSCs into neurons and oligodendrocytes. Additional RNA-sequencing and bioinformatics analyses revealed that genes deregulated by H19 knockdown were involved in transcription, apoptosis, proliferation, cell cycle and response to hypoxia. Western blot analysis validated that loss-of-function and gain-of-function of H19 significantly increased and reduced, respectively, the transcription of cell cycle-related genes including p27. Using ChIRP assay, we found that upregulated H19 in NSCs was physically associated with EZH2 which catalyzes the repressive H3K27me3 histone marker. Knockdown of H19 significantly reduced the enrichment of H3K27me3 at the promoter of p27, leading to the upregulation of p27 expression and consequently inhibition of NSC proliferation. Conclusions: H19 mediates stroke-induced neurogenesis by regulating genes involved in cell cycle and survival through the interaction with chromatin remodeling proteins. Our data provide novel insights into epigenetic regulation of gene expression by lncRNA in neurogenesis.

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