Mammalian genome : official journal of the International Mammalian Genome Society最新文献_第4页

Murine allele and transgene symbols: ensuring unique, concise, and informative nomenclature. 小鼠等位基因和转基因符号:确保独特、简洁和信息丰富的命名法。

IF 2.5

Mammalian genome : official journal of the International Mammalian Genome Society Pub Date : 2022-03-01 Epub Date: 2021-08-14 DOI: 10.1007/s00335-021-09902-3

M N Perry, C L Smith

{"title":"Murine allele and transgene symbols: ensuring unique, concise, and informative nomenclature.","authors":"M N Perry, C L Smith","doi":"10.1007/s00335-021-09902-3","DOIUrl":"https://doi.org/10.1007/s00335-021-09902-3","url":null,"abstract":"In addition to naturally occurring sequence variation and spontaneous mutations, a wide array of technologies exist for modifying the mouse genome. Standardized nomenclature, including allele, transgene, and other mutation nomenclature, as well as persistent unique identifiers (PUID) are critical for effective scientific communication, comparison of results, and integration of data into knowledgebases such as Mouse Genome Informatics (MGI), Alliance for Genome Resources, and International Mouse Strain Resource (IMSR). As well as being the authoritative source for mouse gene, allele, and strain nomenclature, MGI integrates published and unpublished genomic, phenotypic, and expression data while linking to other online resources for a complete view of the mouse as a valuable model organism. The International Committee on Standardized Genetic Nomenclature for Mice has developed allele nomenclature rules and guidelines that take into account the number of genes impacted, the method of allele generation, and the nature of the sequence alteration. To capture details that cannot be included in allele symbols, MGI has further developed allele to gene relationships using sequence ontology (SO) definitions for mutations that provide links between alleles and the genes affected. MGI is also using (HGVS) variant nomenclature for variants associated with alleles that will enhance searching for mutations and will improve cross-species comparison. With the ability to assign unique and informative symbols as well as to link alleles with more than one gene, allele and transgene nomenclature rules and guidelines provide an unambiguous way to represent alterations in the mouse genome and facilitate data integration among multiple resources such the Alliance of Genome Resources and International Mouse Strain Resource.","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"108-119"},"PeriodicalIF":2.5,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s00335-021-09902-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39309152","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}

引用次数: 1

The Rat Genome Database (RGD) facilitates genomic and phenotypic data integration across multiple species for biomedical research. 大鼠基因组数据库(RGD)促进了多物种生物医学研究的基因组和表型数据整合。

IF 2.5

Mammalian genome : official journal of the International Mammalian Genome Society Pub Date : 2022-03-01 Epub Date: 2021-11-05 DOI: 10.1007/s00335-021-09932-x

M L Kaldunski, J R Smith, G T Hayman, K Brodie, J L De Pons, W M Demos, A C Gibson, M L Hill, M J Hoffman, L Lamers, S J F Laulederkind, H S Nalabolu, K Thorat, J Thota, M Tutaj, M A Tutaj, M Vedi, S J Wang, S Zacher, M R Dwinell, A E Kwitek

{"title":"The Rat Genome Database (RGD) facilitates genomic and phenotypic data integration across multiple species for biomedical research.","authors":"M L Kaldunski, J R Smith, G T Hayman, K Brodie, J L De Pons, W M Demos, A C Gibson, M L Hill, M J Hoffman, L Lamers, S J F Laulederkind, H S Nalabolu, K Thorat, J Thota, M Tutaj, M A Tutaj, M Vedi, S J Wang, S Zacher, M R Dwinell, A E Kwitek","doi":"10.1007/s00335-021-09932-x","DOIUrl":"https://doi.org/10.1007/s00335-021-09932-x","url":null,"abstract":"Model organism research is essential for discovering the mechanisms of human diseases by defining biologically meaningful gene to disease relationships. The Rat Genome Database (RGD, ( https://rgd.mcw.edu )) is a cross-species knowledgebase and the premier online resource for rat genetic and physiologic data. This rich resource is enhanced by the inclusion and integration of comparative data for human and mouse, as well as other human disease models including chinchilla, dog, bonobo, pig, 13-lined ground squirrel, green monkey, and naked mole-rat. Functional information has been added to records via the assignment of annotations based on sequence similarity to human, rat, and mouse genes. RGD has also imported well-supported cross-species data from external resources. To enable use of these data, RGD has developed a robust infrastructure of standardized ontologies, data formats, and disease- and species-centric portals, complemented with a suite of innovative tools for discovery and analysis. Using examples of single-gene and polygenic human diseases, we illustrate how data from multiple species can help to identify or confirm a gene as involved in a disease and to identify model organisms that can be studied to understand the pathophysiology of a gene or pathway. The ultimate aim of this report is to demonstrate the utility of RGD not only as the core resource for the rat research community but also as a source of bioinformatic tools to support a wider audience, empowering the search for appropriate models for human afflictions.","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"66-80"},"PeriodicalIF":2.5,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8570235/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39594632","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}

引用次数: 1

Pleiotropy data resource as a primer for investigating co-morbidities/multi-morbidities and their role in disease. 多效性数据资源作为调查共病/多病及其在疾病中的作用的引物。

IF 2.5

Mammalian genome : official journal of the International Mammalian Genome Society Pub Date : 2022-03-01 Epub Date: 2021-09-15 DOI: 10.1007/s00335-021-09917-w

Violeta Muñoz-Fuentes, Hamed Haselimashhadi, Luis Santos, Henrik Westerberg, Helen Parkinson, Jeremy Mason

{"title":"Pleiotropy data resource as a primer for investigating co-morbidities/multi-morbidities and their role in disease.","authors":"Violeta Muñoz-Fuentes, Hamed Haselimashhadi, Luis Santos, Henrik Westerberg, Helen Parkinson, Jeremy Mason","doi":"10.1007/s00335-021-09917-w","DOIUrl":"https://doi.org/10.1007/s00335-021-09917-w","url":null,"abstract":"Most current biomedical and protein research focuses only on a small proportion of genes, which results in a lost opportunity to identify new gene-disease associations and explore new opportunities for therapeutic intervention. The International Mouse Phenotyping Consortium (IMPC) focuses on elucidating gene function at scale for poorly characterized and/or under-studied genes. A key component of the IMPC initiative is the implementation of a broad phenotyping pipeline, which is facilitating the discovery of pleiotropy. Characterizing pleiotropy is essential to identify gene-disease associations, and it is of particular importance when elucidating the genetic causes of syndromic disorders. Here we show how the IMPC is effectively uncovering pleiotropy and how the new mouse models and gene function hypotheses generated by the IMPC are increasing our understanding of the mammalian genome, forming the basis of new research and identifying new gene-disease associations.","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"135-142"},"PeriodicalIF":2.5,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8913486/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39418108","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}

引用次数: 2

Mouse Genome Informatics (MGI): latest news from MGD and GXD. 小鼠基因组信息学(MGI): MGD和GXD的最新消息。

IF 2.5

Mammalian genome : official journal of the International Mammalian Genome Society Pub Date : 2022-03-01 Epub Date: 2021-10-26 DOI: 10.1007/s00335-021-09921-0

Martin Ringwald, Joel E Richardson, Richard M Baldarelli, Judith A Blake, James A Kadin, Cynthia Smith, Carol J Bult

{"title":"Mouse Genome Informatics (MGI): latest news from MGD and GXD.","authors":"Martin Ringwald, Joel E Richardson, Richard M Baldarelli, Judith A Blake, James A Kadin, Cynthia Smith, Carol J Bult","doi":"10.1007/s00335-021-09921-0","DOIUrl":"https://doi.org/10.1007/s00335-021-09921-0","url":null,"abstract":"The Mouse Genome Informatics (MGI) database system combines multiple expertly curated community data resources into a shared knowledge management ecosystem united by common metadata annotation standards. MGI's mission is to facilitate the use of the mouse as an experimental model for understanding the genetic and genomic basis of human health and disease. MGI is the authoritative source for mouse gene, allele, and strain nomenclature and is the primary source of mouse phenotype annotations, functional annotations, developmental gene expression information, and annotations of mouse models with human diseases. MGI maintains mouse anatomy and phenotype ontologies and contributes to the development of the Gene Ontology and Disease Ontology and uses these ontologies as standard terminologies for annotation. The Mouse Genome Database (MGD) and the Gene Expression Database (GXD) are MGI's two major knowledgebases. Here, we highlight some of the recent changes and enhancements to MGD and GXD that have been implemented in response to changing needs of the biomedical research community and to improve the efficiency of expert curation. MGI can be accessed freely at http://www.informatics.jax.org .","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"4-18"},"PeriodicalIF":2.5,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8913530/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39558913","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}

引用次数: 25

The circular RNA circCRIM1 inhibits osteosarcoma progression through sponging miR-513. 环状RNA circrim1通过海绵化miR-513抑制骨肉瘤的进展。

IF 2.5

Mammalian genome : official journal of the International Mammalian Genome Society Pub Date : 2021-12-01 Epub Date: 2021-09-03 DOI: 10.1007/s00335-021-09903-2

Pengfei Wu, Yinghui Kong, Zhitang Dai, Weidong Liu, Zexue Zhao

{"title":"The circular RNA circCRIM1 inhibits osteosarcoma progression through sponging miR-513.","authors":"Pengfei Wu, Yinghui Kong, Zhitang Dai, Weidong Liu, Zexue Zhao","doi":"10.1007/s00335-021-09903-2","DOIUrl":"https://doi.org/10.1007/s00335-021-09903-2","url":null,"abstract":"Numerous studies have suggested that the abnormal expression of circular RNAs plays an essential role in the pathological progression of numerous tumors. Nonetheless, the functions and underlying mechanisms of the circular RNA circCRIM1 in osteosarcoma (OS) are still not fully understood. In this study, 47 classes of OS tissues and adjoining normal tissues were obtained from patients. Real-time PCR was employed to measure circCRIM1 expression levels in both OS tissues and cell lines. The proliferation, migration, and invasion ability in OS cell lines were measured by MTT assays, EDU assays, transwell migration experiments, and transwell invasion assays. The results demonstrated that the expression of circCRIM1 was notably decreased both in OS tissues and cell lines. Depressed circCRIM1 expression was correlated with lymph node metastasis, advanced FIGO stage, and low overall survival of OS patients. In addition, the results indicated that circCRIM1 could decrease the migration, invasion, and growth of OS cells. Further mechanistic studies indicated that circCRIM1 served as a competing endogenous RNA (ceRNA) of miR-513, leading to decreases in the proliferation, migration, and invasion of OS cells. Taken together, our data uncovered a significant role of the circCRIM1/miR-513 pathway in the proliferation, migration, and invasion of OS cell lines and suggested that circCRIM1 may serve as a possible therapeutic target for OS treatment.","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"495-502"},"PeriodicalIF":2.5,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39382312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

LncRNA DRAIR is a novel prognostic and diagnostic biomarker for gastric cancer. LncRNA DRAIR是一种新的胃癌预后和诊断生物标志物。

IF 2.5

Mammalian genome : official journal of the International Mammalian Genome Society Pub Date : 2021-12-01 Epub Date: 2021-09-11 DOI: 10.1007/s00335-021-09911-2

Tian Jin

{"title":"LncRNA DRAIR is a novel prognostic and diagnostic biomarker for gastric cancer.","authors":"Tian Jin","doi":"10.1007/s00335-021-09911-2","DOIUrl":"https://doi.org/10.1007/s00335-021-09911-2","url":null,"abstract":"LncRNA diabetes regulated anti-inflammatory RNA (DRAIR) has been reported to be involved in diabetes-induced injury. However, its role in other human diseases is unclear. Our preliminary sequencing analysis showed its expression was altered in gastric cancer (GC). Thus, this study aimed to explore its diagnostic and prognostic values in GC. DRAIR expression in paired tumor and non-tumor tissues and plasma of GC patients and control samples was determined by RT-qPCR. The diagnostic value of DRAIR for early-stage GC was analyzed using ROC curve analysis. The prognostic value of DRAIR was explored by performing a follow-up (5-year) study. DRAIR expression was downregulated in GC tissues than in non-tumor tissues and in plasma of GC patients than in plasma of healthy controls. DRAIR expression in tumor tissues was closely and positively correlated with its expression in plasma. Plasma DRAIR effectively separated GC patients from controls. High DRAIR levels in tumor tissues and plasma samples were closely correlated with poor survival of GC patients. DRAIR is overexpressed in GC and may serve as an early diagnostic and prognostic biomarker for GC.","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"503-507"},"PeriodicalIF":2.5,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39407851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

Circular RNA circNRIP1 plays oncogenic roles in the progression of osteosarcoma. 环状RNA circNRIP1在骨肉瘤的进展中起致癌作用。

IF 2.5

Mammalian genome : official journal of the International Mammalian Genome Society Pub Date : 2021-12-01 Epub Date: 2021-07-10 DOI: 10.1007/s00335-021-09891-3

Yibin Meng, DingJun Hao, YunFei Huang, ShuaiJun Jia, JiaNan Zhang, XiRui He, Deyin Liu, Liang Sun

{"title":"Circular RNA circNRIP1 plays oncogenic roles in the progression of osteosarcoma.","authors":"Yibin Meng, DingJun Hao, YunFei Huang, ShuaiJun Jia, JiaNan Zhang, XiRui He, Deyin Liu, Liang Sun","doi":"10.1007/s00335-021-09891-3","DOIUrl":"https://doi.org/10.1007/s00335-021-09891-3","url":null,"abstract":"Osteosarcoma (OS) is the most common malignant bone tumor in children and adolescents. Increasing evidence suggests that aberrant expression of circRNAs is associated with the occurrence and progression of many cancers. Here, we investigated the role of circNRIP1 in osteosarcoma and explored its possible underlying mechanisms. Three pairs of osteosarcoma tissues and adjacent normal tissues were applied to the detection of altered expression of circRNAs through circRNAs microarray. And the level of circNRIP1 expression was elevated in osteosarcoma tissues. Compared with that in adjacent normal tissue, circNRIP1 expression level was obviously elevated in 100 osteosarcoma tissues. Besides, circNRIP1 knockdown inhibited proliferation and migration, promoted apoptosis of osteosarcoma cells. Bioinformatic analysis demonstrated circNRIP1 contributed to FOXC2 expression by sponging miR-199a. Furthermore, METTL3 elevated circNRIP1 expression level via m6A modification. In short, METTL3-induced circNRIP1 exerted an oncogenic role in osteosarcoma by sponging miR-199a, which may provide new ideas for the treatment of osteosarcoma.","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"448-456"},"PeriodicalIF":2.5,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s00335-021-09891-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39171063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 15

TUG1 knockdown suppresses cardiac fibrosis after myocardial infarction. TUG1敲低抑制心肌梗死后心肌纤维化。

IF 2.5

Mammalian genome : official journal of the International Mammalian Genome Society Pub Date : 2021-12-01 Epub Date: 2021-08-03 DOI: 10.1007/s00335-021-09895-z

Qingsong Sun, Man Luo, Zhiwei Gao, Xiang Han, Zhuan Yan, Shouxiang Xie, Hongmei Zhao, Hong Sun

{"title":"TUG1 knockdown suppresses cardiac fibrosis after myocardial infarction.","authors":"Qingsong Sun, Man Luo, Zhiwei Gao, Xiang Han, Zhuan Yan, Shouxiang Xie, Hongmei Zhao, Hong Sun","doi":"10.1007/s00335-021-09895-z","DOIUrl":"https://doi.org/10.1007/s00335-021-09895-z","url":null,"abstract":"Cardiac fibrosis is involved in myocardial remodeling following acute myocardial infarction (AMI), which can result in heart failure, arrhythmias and even sudden cardiac death. Investigating the molecular mechanisms of cardiac fibrosis in acute myocardial infarction (AMI) is essential for better understanding this pathology. The current study aims to investigate the effect of TUG1 on cardiac fibrosis after AMI and elucidated the underlying molecular mechanism of AMI. Rats were randomly divided into four groups (sham-operation group, myocardial infarction group (AMI group), si-NC treated group and si-TUG1 treated group). The biological behavior of cardiac fibroblasts treated with TGF-β1after being transfected by si-TUG1 or miR-590 mimic or miR-590 inhibitor or FGF1 mimic or a combination was evaluated using the cell counting kit-8 (CCK8) and Transwell assays. SatarBase v2.0 was used to predict the target microRNAs binding site candidates with TUG1 and FGF1. Western blot and recovery experiments were used to explore the potential mechanism. TUG1 expression was up-regulated and knockdown of TUG1 improved cardiac function in AMI rats. Knockdown of TUG1 suppressed cell viability and migration and improved collagen production of TGF-β1 treated cardiac fibroblasts. SatarBase v2.0 showed TUG1 served as a sponge for miR-590 and FGF1 is a direct target of miR-590. TUG1 expression was increased in AMI tissue and cardiac fibroblasts treated with TGF-β1. TUG1 knockdown suppressed the biological process of cardiac fibroblasts treated with TGF-β1 by sponging miR-590.","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"435-442"},"PeriodicalIF":2.5,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s00335-021-09895-z","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39270254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

Knockdown of lncRNA LUCAT1 attenuates sepsis‑induced myocardial cell injury by sponging miR-642a. lncRNA LUCAT1的敲低通过海绵miR-642a减轻脓毒症诱导的心肌细胞损伤。

IF 2.5

Mammalian genome : official journal of the International Mammalian Genome Society Pub Date : 2021-12-01 Epub Date: 2021-07-17 DOI: 10.1007/s00335-021-09890-4

Jing Wang, Shaobin Xin, Rui Yang, Jiawei Jiang, Youjie Qiao

{"title":"Knockdown of lncRNA LUCAT1 attenuates sepsis‑induced myocardial cell injury by sponging miR-642a.","authors":"Jing Wang, Shaobin Xin, Rui Yang, Jiawei Jiang, Youjie Qiao","doi":"10.1007/s00335-021-09890-4","DOIUrl":"https://doi.org/10.1007/s00335-021-09890-4","url":null,"abstract":"The heart is one of the most common organs involved in sepsis-induced organ dysfunction and about 50% septic patients complicated with myocardial injury. So far, the molecular mechanisms underlying sepsis-induced cardiac damage remain unclear. In this study we aimed to evaluate the effect of miR-642a on sepsis-induced cardiac injury in vitro and explore the possible lncRNA-microRNA mechanism. We first downloaded GSE101639 to identify differentially expressed genes (DEGs) in sepsis. The expression of miR-642a in LPS-induced H9C2 cells was detected by qRT-PCR. MTT assay, cell migration, flow cytometry analysis, ELISA, qRT-PCR and Western blotting analysis were applied to evaluating the effect of miR-642a mimic on LPS-induced H9C2 cells. The bioinformatics analysis and the rescue experiment were devoted to the underlying mechanism. The results showed miR-642a expression was decreased in septic patients and LPS-induced H9C2 cells. Besides, MiR-642a mimic promoted cell viability and migration, inhibited cell apoptosis of LPS-induced H9C2 cells. Bioinformatics analysis showed miR-642a directly targets with 3'-UTR of ROCK1. Moreover, LUCAT1 regulated ROCK1 expression act as a competing endogenous RNA (ceRNA) for miR-642a. Our data demonstrated that lncRNA LUCAT1 could function via sponging miR-642a to regulate ROCK1 expression in LPS-induced H9C2 cells. And knockdown of lncRNA LUCAT1 could suppress LPS-induced cardiac injury in vitro.","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"457-465"},"PeriodicalIF":2.5,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s00335-021-09890-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39192954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6

The calcimedin annexin A3 displays tumor-promoting effect in esophageal squamous cell carcinoma by activating NF-κB signaling. 钙钙蛋白膜联蛋白A3通过激活NF-κB信号通路在食管鳞状细胞癌中显示促瘤作用。

IF 2.5

Mammalian genome : official journal of the International Mammalian Genome Society Pub Date : 2021-10-01 Epub Date: 2021-06-09 DOI: 10.1007/s00335-021-09883-3

Shihao Gao, Zhangzhan Wang, Xiaozhe Liu, Bing Xu, Fengjin Liu

{"title":"The calcimedin annexin A3 displays tumor-promoting effect in esophageal squamous cell carcinoma by activating NF-κB signaling.","authors":"Shihao Gao, Zhangzhan Wang, Xiaozhe Liu, Bing Xu, Fengjin Liu","doi":"10.1007/s00335-021-09883-3","DOIUrl":"https://doi.org/10.1007/s00335-021-09883-3","url":null,"abstract":"Esophageal squamous cell carcinoma (ESCC) is one of the lethal malignancies commonly found in the eastern world, with overall five-year survival rates less than 25%. The present study aimed to investigate the biological function of annexin A3 (ANXA3) in ESCC cell proliferation. The mRNA and protein levels of ANXA3 in ESCC tissues and cell lines were determined by real-time PCR and Western blot, respectively. Lentiviral transduction was applied to overexpress or reduce ANXA3 expression in ESCC cell lines. The effect of ANXA3 on ESCC cell proliferation was evaluated by cell-counting kit-8 assay in vitro and tumor-bearing animal model in vivo. We found that ANXA3 was substantially upregulated in ESCC tissues compared to adjacent normal tissues as well as ESCC cell lines compared to normal esophageal endothelial cells. Suppression of ANXA3 significantly inhibited ESCC cell proliferation in vitro and tumor growth in vivo. We further revealed that NF-κB was involved in ANXA3-mediated ESCC cell proliferation. Our results suggest that ANXA3 acts as an oncogene in ESCC, and targeting ANXA3 or NF-κB may serve as potential therapeutic strategies for patients with ESCC.","PeriodicalId":412165,"journal":{"name":"Mammalian genome : official journal of the International Mammalian Genome Society","volume":" ","pages":"381-388"},"PeriodicalIF":2.5,"publicationDate":"2021-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/s00335-021-09883-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39011695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2