Non-Coding RNA最新文献

{"title":"Phosphate Deficiency: A Tale from the End of PILNCR2.","authors":"Santosh Kumar Upadhyay","doi":"10.3390/ncrna9040040","DOIUrl":"https://doi.org/10.3390/ncrna9040040","url":null,"abstract":"<p><p>A deficiency in inorganic phosphate (Pi) induces the expression of miRNA399 and the accumulation of its target Pi transporters (<i>PHT1s</i>) mRNA, which is contrary to the goal of miRNA-mediated gene regulation. Recently, a novel mechanism of RNA/RNA-duplex formation between the transcripts of a Pi deficiency-induced long non-coding RNA (<i>PILNCR2</i>) and <i>PHT1s</i> has been reported, which prevents the binding and cleavage of miRNA399 to <i>PHT1</i> mRNAs, thereby providing tolerance of Pi-deficient conditions. Moreover, the way in which ribosomes move through the RNA/RNA-duplex for the translation of PHT1 transporter proteins remains elusive.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"9 4","pages":""},"PeriodicalIF":4.3,"publicationDate":"2023-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10457764/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10071698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DoxoDB: A Database for the Expression Analysis of Doxorubicin-Induced lncRNA Genes.","authors":"Rebecca Distefano,&nbsp;Mirolyuba Ilieva,&nbsp;Jens Hedelund Madsen,&nbsp;Sarah Rennie,&nbsp;Shizuka Uchida","doi":"10.3390/ncrna9040039","DOIUrl":"https://doi.org/10.3390/ncrna9040039","url":null,"abstract":"<p><p>Cancer and cardiovascular disease are the leading causes of death worldwide. Recent evidence suggests that these two life-threatening diseases share several features in disease progression, such as angiogenesis, fibrosis, and immune responses. This has led to the emergence of a new field called cardio-oncology. Doxorubicin is a chemotherapy drug widely used to treat cancer, such as bladder and breast cancer. However, this drug causes serious side effects, including acute ventricular dysfunction, cardiomyopathy, and heart failure. Based on this evidence, we hypothesize that comparing the expression profiles of cells and tissues treated with doxorubicin may yield new insights into the adverse effects of the drug on cellular activities. To test this hypothesis, we analyzed published RNA sequencing (RNA-seq) data from doxorubicin-treated cells to identify commonly differentially expressed genes, including long non-coding RNAs (lncRNAs) as they are known to be dysregulated in diseased tissues and cells. From our systematic analysis, we identified several doxorubicin-induced genes. To confirm these findings, we treated human cardiac fibroblasts with doxorubicin to record expression changes in the selected doxorubicin-induced genes and performed a loss-of-function experiment of the lncRNA <i>MAP3K4-AS1</i>. To further disseminate the analyzed data, we built the web database DoxoDB.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"9 4","pages":""},"PeriodicalIF":4.3,"publicationDate":"2023-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10366827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9874674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functions of Circular RNA in Human Diseases and Illnesses.","authors":"Alison Gu,&nbsp;Dabbu Kumar Jaijyan,&nbsp;Shaomin Yang,&nbsp;Mulan Zeng,&nbsp;Shaokai Pei,&nbsp;Hua Zhu","doi":"10.3390/ncrna9040038","DOIUrl":"https://doi.org/10.3390/ncrna9040038","url":null,"abstract":"<p><p>Circular RNAs (circRNAs) represent single-stranded RNA species that contain covalently closed 3' and 5' ends that provide them more stability than linear RNA, which has free ends. Emerging evidence indicates that circRNAs perform essential functions in many DNA viruses, including coronaviruses, Epstein-Barr viruses, cytomegalovirus, and Kaposi sarcoma viruses. Recent studies have confirmed that circRNAs are present in viruses, including DNA and RNA viruses, and play various important functions such as evading host immune response, disease pathogenesis, protein translation, miRNA sponges, regulating cell proliferation, and virus replication. Studies have confirmed that circRNAs can be biological signatures or pathological markers for autoimmune diseases, neurological diseases, and cancers. However, our understanding of circRNAs in DNA and RNA viruses is still limited, and functional evaluation of viral and host circRNAs is essential to completely understand their biological functions. In the present review, we describe the metabolism and cellular roles of circRNA, including its roles in various diseases and viral and cellular circRNA functions. Circular RNAs are found to interact with RNA, proteins, and DNA, and thus can modulate cellular processes, including translation, transcription, splicing, and other functions. Circular RNAs interfere with various signaling pathways and take part in vital functions in various biological, physiological, cellular, and pathophysiological processes. We also summarize recent evidence demonstrating cellular and viral circRNA's roles in DNA and RNA viruses in this growing field of research.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"9 4","pages":""},"PeriodicalIF":4.3,"publicationDate":"2023-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10366867/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9874675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA Functional Screening in Organismal Development.","authors":"Yang Li,&nbsp;Huicong Zhai,&nbsp;Lingxiu Tong,&nbsp;Cuicui Wang,&nbsp;Zhiming Xie,&nbsp;Ke Zheng","doi":"10.3390/ncrna9040036","DOIUrl":"https://doi.org/10.3390/ncrna9040036","url":null,"abstract":"<p><p>Controversy continues over the functional prevalence of long non-coding RNAs (lncRNAs) despite their being widely investigated in all kinds of cells and organisms. In animals, lncRNAs have aroused general interest from exponentially increasing transcriptomic repertoires reporting their highly tissue-specific and developmentally dynamic expression, and more importantly, from growing experimental evidence supporting their functionality in facilitating organogenesis and individual fitness. In mammalian testes, while a great multitude of lncRNA species are identified, only a minority of them have been shown to be useful, and even fewer have been demonstrated as true requirements for male fertility using knockout models to date. This noticeable gap is attributed to the virtual existence of a large number of junk lncRNAs, the lack of an ideal germline culture system, difficulty in loss-of-function interrogation, and limited screening strategies. Facing these challenges, in this review, we discuss lncRNA functionality in organismal development and especially in mouse testis, with a focus on lncRNAs with functional screening.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"9 4","pages":""},"PeriodicalIF":4.3,"publicationDate":"2023-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10366883/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9865986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impacts of MicroRNA-483 on Human Diseases.","authors":"Katy Matson, Aaron Macleod, Nirali Mehta, Ellie Sempek, Xiaoqing Tang","doi":"10.3390/ncrna9040037","DOIUrl":"10.3390/ncrna9040037","url":null,"abstract":"<p><p>MicroRNAs (miRNAs) are short non-coding RNA molecules that regulate gene expression by targeting specific messenger RNAs (mRNAs) in distinct cell types. This review provides a com-prehensive overview of the current understanding regarding the involvement of miR-483-5p and miR-483-3p in various physiological and pathological processes. Downregulation of miR-483-5p has been linked to numerous diseases, including type 2 diabetes, fatty liver disease, diabetic nephropathy, and neurological injury. Accumulating evidence indicates that miR-483-5p plays a crucial protective role in preserving cell function and viability by targeting specific transcripts. Notably, elevated levels of miR-483-5p in the bloodstream strongly correlate with metabolic risk factors and serve as promising diagnostic markers. Consequently, miR-483-5p represents an appealing biomarker for predicting the risk of developing diabetes and cardiovascular diseases and holds potential as a therapeutic target for intervention strategies. Conversely, miR-483-3p exhibits significant upregulation in diabetes and cardiovascular diseases and has been shown to induce cellular apoptosis and lipotoxicity across various cell types. However, some discrepancies regarding its precise function have been reported, underscoring the need for further investigation in this area.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"9 4","pages":""},"PeriodicalIF":3.6,"publicationDate":"2023-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10366739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9874680","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Small Nucleolar (Sno)RNA: Therapy Lays in Translation.","authors":"Ofri Rabany,&nbsp;Daphna Nachmani","doi":"10.3390/ncrna9030035","DOIUrl":"https://doi.org/10.3390/ncrna9030035","url":null,"abstract":"<p><p>The ribosome is one of the largest complexes in the cell. Adding to its complexity are more than 200 RNA modification sites present on ribosomal RNAs (rRNAs) in a single human ribosome. These modifications occur in functionally important regions of the rRNA molecule, and they are vital for ribosome function and proper gene expression. Until recent technological advancements, the study of rRNA modifications and their profiles has been extremely laborious, leaving many questions unanswered. Small nucleolar RNAs (snoRNAs) are non-coding RNAs that facilitate and dictate the specificity of rRNA modification deposition, making them an attractive target for ribosome modulation. Here, we propose that through the mapping of rRNA modification profiles, we can identify cell-specific modifications with high therapeutic potential. We also describe the challenges of achieving the targeting specificity needed to implement snoRNAs as therapeutic targets in cancers.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"9 3","pages":""},"PeriodicalIF":4.3,"publicationDate":"2023-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10301893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10078236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Review of IsomiRs in Colorectal Cancer.","authors":"Molly A Lausten, Bruce M Boman","doi":"10.3390/ncrna9030034","DOIUrl":"10.3390/ncrna9030034","url":null,"abstract":"<p><p>As advancements in sequencing technology rapidly continue to develop, a new classification of microRNAs has occurred with the discovery of isomiRs, which are relatively common microRNAs with sequence variations compared to their established template microRNAs. This review article seeks to compile all known information about isomiRs in colorectal cancer (CRC), which has not, to our knowledge, been gathered previously to any great extent. A brief overview is given of the history of microRNAs, their implications in colon cancer, the canonical pathway of biogenesis and isomiR classification. This is followed by a comprehensive review of the literature that is available on microRNA isoforms in CRC. The information on isomiRs presented herein shows that isomiRs hold great promise for translation into new diagnostics and therapeutics in clinical medicine.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"9 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2023-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10300944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9774677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A microRNA Arising from the Negative Strand of SARS-CoV-2 Genome Targets FOS to Reduce AP-1 Activity.","authors":"Francesco Greco,&nbsp;Elisa Lorefice,&nbsp;Claudia Carissimi,&nbsp;Ilaria Laudadio,&nbsp;Fabiola Ciccosanti,&nbsp;Martina Di Rienzo,&nbsp;Francesca Colavita,&nbsp;Silvia Meschi,&nbsp;Fabrizio Maggi,&nbsp;Gian Maria Fimia,&nbsp;Valerio Fulci","doi":"10.3390/ncrna9030033","DOIUrl":"https://doi.org/10.3390/ncrna9030033","url":null,"abstract":"<p><p>Virus-encoded microRNAs were first reported in the Epstein-Barr virus in 2004. Subsequently, a few hundred viral miRNAs have been identified, mainly in DNA viruses belonging to the <i>herpesviridae</i> family. To date, only 30 viral miRNAs encoded by RNA viruses are reported by miRBase. Since the outbreak of the SARS-CoV-2 pandemic, several studies have predicted and, in some cases, experimentally validated miRNAs originating from the positive strand of the SARS-CoV-2 genome. By integrating NGS data analysis and qRT-PCR approaches, we found that SARS-CoV-2 also encodes for a viral miRNA arising from the minus (antisense) strand of the viral genome, in the region encoding for ORF1ab, herein referred to as SARS-CoV-2-miR-AS1. Our data show that the expression of this microRNA increases in a time course analysis of SARS-CoV-2 infected cells. Furthermore, enoxacin treatment enhances the accumulation of the mature SARS-CoV-2-miR-AS1 in SARS-CoV-2 infected cells, arguing for a Dicer-dependent processing of this small RNA. In silico analysis suggests that SARS-CoV-2-miR-AS1 targets a set of genes which are translationally repressed during SARS-CoV-2 infection. We experimentally validated that SARS-CoV-2-miR-AS1 targets FOS, thus repressing the AP-1 transcription factor activity in human cells.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"9 3","pages":""},"PeriodicalIF":4.3,"publicationDate":"2023-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10301948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10078238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inverse Impact of Cancer Drugs on Circular and Linear RNAs in Breast Cancer Cell Lines.","authors":"Anna Terrazzan,&nbsp;Francesca Crudele,&nbsp;Fabio Corrà,&nbsp;Pietro Ancona,&nbsp;Jeffrey Palatini,&nbsp;Nicoletta Bianchi,&nbsp;Stefano Volinia","doi":"10.3390/ncrna9030032","DOIUrl":"https://doi.org/10.3390/ncrna9030032","url":null,"abstract":"<p><p>Altered expression of circular RNAs (circRNAs) has previously been investigated in breast cancer. However, little is known about the effects of drugs on their regulation and relationship with the cognate linear transcript (linRNA). We analyzed the dysregulation of both 12 cancer-related circRNAs and their linRNAs in two breast cancer cell lines undergoing various treatments. We selected 14 well-known anticancer agents affecting different cellular pathways and examined their impact. Upon drug exposure circRNA/linRNA expression ratios increased, as a result of the downregulation of linRNA and upregulation of circRNA within the same gene. In this study, we highlighted the relevance of identifying the drug-regulated circ/linRNAs according to their oncogenic or anticancer role. Interestingly, <i>VRK1</i> and <i>MAN1A2</i> were increased by several drugs in both cell lines. However, they display opposite effects, circ/linVRK1 favors apoptosis whereas circ/linMAN1A2 stimulates cell migration, and only XL765 did not alter the ratio of other dangerous circ/linRNAs in MCF-7. In MDA-MB-231 cells, AMG511 and GSK1070916 decreased circGFRA1, as a good response to drugs. Furthermore, some circRNAs might be associated with specific mutated pathways, such as the PI3K/AKT in MCF-7 cells with circ/linHIPK3 correlating to cancer progression and drug-resistance, or NHEJ DNA repair pathway in TP-53 mutated MDA-MB-231 cells.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"9 3","pages":""},"PeriodicalIF":4.3,"publicationDate":"2023-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10204552/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9516158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic Deletion of the <i>LINC00520</i> Homolog in Mouse Aggravates Angiotensin II-Induced Hypertension.","authors":"Xiaofang Tang, Chih-Hung Lai, Naseeb K Malhi, Rahuljeet Chadha, Yingjun Luo, Xuejing Liu, Dongqiang Yuan, Alonso Tapia, Maryam Abdollahi, Guangyu Zhang, Riccardo Calandrelli, Yan-Ting Shiu, Zhao V Wang, June-Wha Rhee, Sheng Zhong, Rama Natarajan, Zhen Bouman Chen","doi":"10.3390/ncrna9030031","DOIUrl":"10.3390/ncrna9030031","url":null,"abstract":"<p><p>(1) Background: Hypertension is a complex, multifactorial disease that is caused by genetic and environmental factors. Apart from genetic predisposition, the mechanisms involved in this disease have yet to be fully understood. We previously reported that LEENE (lncRNA enhancing endothelial nitric oxide expression, transcribed from <i>LINC00520</i> in the human genome) regulates endothelial cell (EC) function by promoting the expression of endothelial nitric oxide synthase (eNOS) and vascular growth factor receptor 2 (VEGFR2). Mice with genetic deletion of the <i>LEENE/LINC00520</i> homologous region exhibited impaired angiogenesis and tissue regeneration in a diabetic hindlimb ischemia model. However, the role of LEENE in blood pressure regulation is unknown. (2) Methods: We subjected mice with genetic ablation of <i>leene</i> and wild-type littermates to Angiotensin II (AngII) and monitored their blood pressure and examined their hearts and kidneys. We used RNA-sequencing to identify potential <i>leene</i>-regulated molecular pathways in ECs that contributed to the observed phenotype. We further performed in vitro experiments with murine and human ECs and ex vivo experiments with murine aortic rings to validate the select mechanism. (3) Results: We identified an exacerbated hypertensive phenotype of <i>leene</i>-KO mice in the AngII model, evidenced by higher systolic and diastolic blood pressure. At the organ level, we observed aggravated hypertrophy and fibrosis in the heart and kidney. Moreover, the overexpression of human LEENE RNA, in part, restored the signaling pathways impaired by <i>leene</i> deletion in murine ECs. Additionally, Axitinib, a tyrosine kinase inhibitor that selectively inhibits VEGFR suppresses LEENE in human ECs. (4) Conclusions: Our study suggests LEENE as a potential regulator in blood pressure control, possibly through its function in ECs.</p>","PeriodicalId":19271,"journal":{"name":"Non-Coding RNA","volume":"9 3","pages":""},"PeriodicalIF":3.6,"publicationDate":"2023-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10204496/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10003333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}