Critical Reviews in Eukaryotic Gene Expression最新文献

{"title":"Discovery of Target Genes for Fibromyalgia through Bioinformatics Analysis.","authors":"Mao Guo, Botao Zhang","doi":"10.1615/CritRevEukaryotGeneExpr.2025057263","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2025057263","url":null,"abstract":"<p><p>Fibromyalgia (FM) is a chronic condition marked by widespread pain, fatigue, and other debilitating symptoms, affecting 2-4% of the population, predominantly women. Diagnosing FM is challenging due to its complex symptoms and lack of specific biomarkers. To characterize the gene expression profile in FM and identify target genes and potential biomarkers for FM. The RNA-sequencing data (RNA-seq) from FM patients and healthy controls were downloaded from the GEO database and analyzed in R to detect differentially expressed genes (DEGs). A weighted gene co-expression network analysis (WGCNA) was conducted on all genes to identify FM-associated modules. The intersection of DEGs with key module genes was used to build four machine learning models, with the top features from the support vector machine model tested for drug sensitivity to identify therapeutic targets. Expression of the top five genes was validated using real-time quantitative polymerase chain reaction and Western blotting. We identified 1599 DEGs between FM and healthy control. WGCNA revealed that 267 genes in the pink module were correlated with FM. The overlapped 76 key DEGs allow us to build machine-learning models that predict FM with high accuracy (area under the curve = 0.877). The top five genes that are contributing to the model were tested for potential drug targets. Drug sensitivity analysis showed a strong correlation between HAVCR1 and 10 tyrosine kinase inhibitors among the top gene-drug relationships. This study identified key FM-associated gene targets, demonstrating that their expression profiles can be used to predict FM risk. Our findings provide insights into the molecular mechanisms of FM and highlight potential therapeutic targets for improved FM treatment.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 4","pages":"39-53"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144060051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL17-Mediated Inhibition of M1 Macrophage Polarization Alleviates the Progression of Ankylosing Spondylitis.","authors":"Jiang-Tao Lv, Ying-Ying Zhang, Shao-Qi Tian, Jiang-Jun Liu","doi":"10.1615/CritRevEukaryotGeneExpr.2024057127","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2024057127","url":null,"abstract":"<p><p>RNA methylation is involved in the pathogenesis of ankylosing spondylitis (AS). This study aimed to investigate the potentials of METTL17 in AS. mRNA expression was detected using RT-qPCR. RNA methylation was detected using MeRIP assay. Protein expression was detected using western blot. Cell proliferation was detected using EdU assay. Macrophage functions was detected using flow cytometry. METTL17 was upregulated after exposure to LPS. However, METTL17 knockdown promoted inflammatory response. Moreover, METTL17 knockdown promoted M1 macrophage polarization. Mechanically, METTL17 regulate RNA methylation. Mechanically, METTL17 promoted the RNA methylation of STAT1, inhibiting the mRNA and protein stability of STAT1. In summary, METTL17 inhibits inflammatory response and M1 macrophage polarization via mediating the RNA methylation of STAT1. Therefore, targeting METTL17/STAT1 may be a promising strategy for AS.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 2","pages":"87-95"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plumbagin Induces Apoptosis in Diffuse Large B-Cell Lymphoma by Modulating the ROS-PI3K-Akt-mTOR Signaling Pathway.","authors":"Jingfang Du, Tao Ye, Pian Li, Yanfang Yu, Fengli Fan, Ruiying Zhang, Na Shen","doi":"10.1615/CritRevEukaryotGeneExpr.2024055447","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2024055447","url":null,"abstract":"<p><p>This study aimed to investigate the potential effects and underlying mechanism of plumbagin (PL) on the proliferation and apoptosis of SU-DHL-4 cells, a type of diffuse large B-cell lymphoma (DLBCL), through in vitro and in vivo experiments. The in vitro experiments were performed by subjecting SU-DHL-4 cells to different concentrations of PL. The proliferation rate of the cells was evaluated using the CCK8 assay. Flow cytometry, quantitative real-time polymerase chain reaction (qRT-PCR), and a commercial ROS detection kit were employed to quantify the apoptosis rate, the antioxidant enzyme activity, and the levels of reactive oxygen species (ROS), respectively. The protein expression of Bax, BCL2, caspase-3, cleaved caspase-3, PI3K, p-PI3K, Akt, p-Akt, mTOR, and p-mTOR were determined by western blotting. The cell-derived tumor xenograft tumor model was constructed by subcutaneously injecting SU-DHL-4 cells into NOD-SCID mice. The therapeutic effect of PL was then evaluated by morphological staining. Results from the in vitro experiments demonstrated that PL could effectively inhibit cell proliferation, increase the production of reactive oxygen species (ROS), and induce apoptosis in SU-DHL-4 cells in both a time- and a dosage-dependent manner. Furthermore, PL treatment upregulated the protein expression of Bax and cleaved caspase-3 (P < 0.05). In parallel, PL treatment concurrently DOWNREGULATED the protein expression of Bcl-2, p-PI3K, p-Akt, and p-mTOR (P < 0.05). More important, it inhibits the growth of mouse xenograft tumors. PL promotes apoptosis of DLBCL cells, potentially by upregulating ROS and suppressing the PI3K/Akt/mTOR signaling pathway. These findings might be a useful reference for future drug discovery.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 2","pages":"13-25"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and Validation of a Novel Prognostic Signature of Gastric Cancer Based on Seven Complement System-Related Genes: An Integrated Analysis.","authors":"Jiaxing Zhang, Weijing Zhu, Shengrui Yang, Jie Liu, Futian Tang, Yumin Li","doi":"10.1615/CritRevEukaryotGeneExpr.2024057000","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2024057000","url":null,"abstract":"<p><p>The complement system (CS) is linked to the progression of gastric cancer (GC), which has a high mortality rate, though its mechanisms in GC remain unclear. This study aims to identify CS-related prognostic genes with causal links to GC, and to investigate their mechanisms. The intersection between differentially expressed genes (DEGs) obtained from the TCGA-STAD dataset and CS-related genes (CRGs) was defined as differentially expressed CRGs (DCRGs). Prognostic genes with a causal association with GC (pCDCRGs) were sequentially identified via Mendelian randomization (MR) analysis and Cox and least absolute shrinkage and selection operator (LASSO) regression analyses, followed by expression analysis. A gene signature and a nomogram were then established based on pCDCRGs and independent prognostic factors. Subsequent analyses focused on functional enrichment, immune relevance, drug sensitivity, gene interactions, and molecular regulatory networks. Eventually, reverse transcription-quantitative PCR (RT-qPCR) was employed to validate expression of pCDCRGs. DCRGs were obtained from the intersection of 8,418 DEGs and 241 CRGs. Among 12 DCRGs with causal association (CDCRGs) with GC, 7 genes were identified as pCDCRGs, including FANCG, FANCF, F2R, C4BPA, SERPINF2, PROC, and CD59. Notably, CD59 was markedly highly expressed in the normal group, whereas the other genes were markedly highly expressed in the GC group. Afterward, an accurate pCDCRG signature was developed. Risk score, age, and stage were recognized as independent risk factors, and the constructed nomogram demonstrated strong predictive accuracy. Additionally, analyses indicated that these 7 pCDCRGs may influence GC by affecting pathways such as complement and coagulation cascades, immune cell infiltration, immune characteristics, immunotherapy responses, and drug sensitivity. These effects may be linked to gene interactions and the regulatory roles of lncRNAs like RMRP and miRNAs such as hsa-mir-613. RT-qPCR showed C4BPA, PROC, F2R, and SERPINF2 were markedly up-regulated, whereas CD59 was markedly down-regulated in GC tissues. This study identified seven complement system-related prognostic genes with causal links to GC, based on which we developed a highly predictive 7-pCDCRG signature, providing valuable insights for clinical prognostic prediction and immunotherapy in GC patients.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 3","pages":"1-22"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143451133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and Validation of T Cell-Related Hub Biomarkers for Early Diagnosis of Diabetic Kidney Disease Using Single-Cell and Bulk Dataset Analysis.","authors":"Zhenhua Wu, Meifang Ren, Miao Tan, Bing Yang, Suzhi Chen, Fengwen Yang, Guodong Yuan, Jinchuan Tan","doi":"10.1615/CritRevEukaryotGeneExpr.2025056960","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2025056960","url":null,"abstract":"<p><p>Diabetic kidney disease (DKD) is the most common complication of diabetes and a leading cause of chronic kidney disease that frequently leads to end-stage renal disease (ESRD). The pathogenesis of DKD is complex and is not fully understood. This study was designed to identify key targets for DKD diagnosis and explore the underlying molecular mechanisms.</p><p><strong>Methods: </strong>DKD-specific clusters were selected from single-cell datasets. Gene modules were identified using hairpin-dynamic weighted gene co-expression network analysis (hdWGCNA). Multiple machine learning algorithms were applied to model and screen hub genes from two bulk datasets. Rat model of DKD was built using optical microscopes to observe the histopathological changes in the kidney by HE, PAS, and Masson staining. The expression of RASGRP3, PDE3B, and CD247 in DKD-Rat was verified by RT-PCR, and the expression of RASGRP3, PDE3B, and CD247 in the serum samples of DKD patients was verified by ELISA. The results of sex and age, RASGRP3, PDE3B, CD247 were calculated by multivariate logistic regression analysis.</p><p><strong>Results: </strong>Three hub genes were obtained through screening single-cell and two bulk datasets. In-depth exploration of the potential molecular mechanisms of the hub genes was conducted using gene set variation analysis (GSVA), immune infiltration analysis, and single-cell correlation analysis. Receiver operating characteristic (ROC) curve confirmed a high diagnostic value of the hub biomarkers, and a high-efficiency diagnostic model was constructed and mutually validated in the two datasets. We found that damaged tubular number and interstitial fibrotic percentage were significantly increased in DKD rat. As shown by HE, PAS and Masson staining, the mRNA levels of PDE3B and CD247 were markedly upregulated in DKD rat compared with those in the control group. Lower expression levels of RASGRP3 mRNA were manifested in DKD. The levels of RASGRP3, PDE3B, CD247 in DKD patients by ELISA were statistically significant (p < 0.05). PDE3B and CD247 had an AUC value greater than 0.9,RASGRP3 had an AUC value greater than 0.7.</p><p><strong>Conclusion: </strong>This study identified 3 T cell-related hub biomarkers, providing references for the early diagnosis of DKD and changes in T cells during DKD progression.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 4","pages":"65-84"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144056963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Propofol Protects against Pyroptosis of Photoreceptors in Subretinal Hemorrhage via Regulating SIRT6/NLRP3 Signaling.","authors":"Huihui Wang, Limei Zhang, Xiaoli Bai, Hao Wang, Hao Sun","doi":"10.1615/CritRevEukaryotGeneExpr.2024056605","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2024056605","url":null,"abstract":"<p><p>Subretinal hemorrhage-induced neurotoxicity is a key cause of vision loss in age-related macular degeneration (AMD). The purpose of this study is to investigate the effects of Propofol on neurotoxicity. Oxygen glucose deprivation (OGD) was used to establish in vitro subretinal hemorrhage model. Gene expression was determined using reverse transcription-quantitative polymerase chain reaction and western blot. Cytokine release was determined using enzyme-linked immunosorbent assay. The interaction between sirtuin 6 (SIRT6) and NLR family pyrin domain containing 3 (NLRP3) was detected using co-immunoprecipitation assay. Cellular function was determined using cell counting kit-8 assay, lactate dehydrogenase assay, and terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Propofol suppressed the inflammatory response induced by OGD. Moreover, Propofol inhibited the neurotoxicity and pyroptosis of photoreceptors. Propofol mediated the overexpression of SIRT6, which was downregulated in AMD. Inhibition of SIRT6 alleviated its deacetylation of NLRP3. Additionally, SIRT6 deficiency antagonized the effects of Propofol and promoted the neurotoxicity and pyroptosis of photoreceptors. Taken together, Propofol protects against subretinal hemorrhage-induced neurotoxicity and pyroptosis of photoreceptors via promoting SIRT6-mediated deacetylation of NLRP3.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 2","pages":"75-85"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic Signatures and Prognostic Biomarkers Analysis of Methylation-Driven Genes in Uterine Endometrial Carcinosarcoma.","authors":"Na Zhang, Wangshu Li, Fang Wang, Cailing Han, Guijun Li, Liyun Ren, Chen Hua","doi":"10.1615/CritRevEukaryotGeneExpr.2024055577","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2024055577","url":null,"abstract":"<p><p>Uterine corpus endometrial carcinoma (UCEC) is one of the most common gynecological malignancies, and understanding the molecular mechanisms underlying its development is essential for improving diagnosis and treatment. However, the role of DNA methylation, a key epigenetic modification, in UCEC prognosis prediction and clinical treatment strategies has rarely been studied. This study utilized publicly available datasets from The Cancer Genome Atlas (TCGA) and online bioinformatics tools to analyze the differential methylation and expression of six selected genes: TP53, PTEN, PTX3, TNK1, PPP2R1A, and KLRG2. These genes were chosen based on their known roles in cancer-related pathways, previous associations with oncogenic processes, and preliminary data showing significant changes in methylation and expression in UCEC compared with normal tissues. We integrated mRNA expression and DNA methylation data with the MethylMix method to identify genes with methylation-driven expression changes. Our analysis revealed that these genes exhibit distinct differential expression and methylation patterns in UCEC, suggesting potential regulatory mechanisms. The expression patterns across the six genes were observed, and TP53, TNK1, PPP2R1A, and KLRG2 were upregulated in tumors, and PTX3 was downregulated in tumors. At the same time, there was no significant change in the expression of PTEN gene. The differential expression correlates with changes in methylation, providing insights into the gene regulation occurring in UCEC. Additionally, Kaplan-Meier survival analysis revealed that the expression levels of specific genes, particularly PTX3, TNK1, and KLRG1, are significantly associated with overall survival in UCEC patients. Higher expression of these genes correlated with poorer survival outcomes, suggesting their potential as prognostic markers. In contrast, the expression of TP53, PTEN, and PPP2R1A did not show a significant impact on patient survival. The functional importance of these genes was investigated utilizing pathway enrichment and protein-protein interaction networks. Additionally, pathway enrichment analysis indicated these genes are involved in critical cancer pathways. The findings highlight the importance of integrating epigenetic and transcriptomic data to understand UCEC pathogenesis and suggest that the identified genes could serve as potential biomarkers for early diagnosis and treatment strategies.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 2","pages":"27-47"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CircCNKSR2 Facilitates NSCLC Tumorigenesis and Warburg Effect via miRNA-138-5p/PLEK2 Axis.","authors":"Dongxiao Ding, Ke Shi, Junjie Ying, Wenjun Shang, Chengli Du","doi":"10.1615/CritRevEukaryotGeneExpr.2024055827","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2024055827","url":null,"abstract":"<p><p>Non-small cell lung cancer (NSCLC) has a high global incidence and mortality rate. Although circRNAs have significant attention in tumor research, it's role in NSCLC is uncertain. QRT-PCR and Western blotting were utilized to quantify the expression of circCNKSR2, miR-138-5p, and PLEK2 in NSCLC tissues and cells. The characteristics and subcellular localization of circCNKSR2 were determined using RNase R analysis and qRT-PCR. In vitro functional experiments determined the biological functions of circCNKSR2. The specific binding interactions among circCNKSR2, miR-138-5p, and PLEK2 were evaluated through bioinformatics analysis, luciferase reporter, and rescue assays. In vivo xenograft model was established to examine the impact of circCNKSR2, which was significantly increased in NSCLC tissues and cells. Functional studies demonstrated that silencing circCNKSR2 significantly inhibited NSCLC malignant phenotype and Warburg effect. Bioinformatics analysis and rescue experiments verification indicated circCNKSR2 functioned as a miR-138-5p sponge, and inhibiting miR-138-5p reversed the suppressive effect of silencing circCNKSR2 in NSCLC. Additionally, PLEK2 identified as a miR-138-5p target gene. The potential regulatory role of circCNKSR2 in NSCLC progression and Warburg effect via the miR-138-5p/PLEK2 pathway was demonstrated.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 2","pages":"49-63"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical characteristics and gene analysis in 7 Chinese children with cystic fibrosis.","authors":"Chunyan Guo, Xing Chen, Fengqin Liu, Yan Liang, Juan Yang, Fangfang Dai, Ning Ding, Ke Wang, Jing Zhang","doi":"10.1615/CritRevEukaryotGeneExpr.2025057731","DOIUrl":"https://doi.org/10.1615/CritRevEukaryotGeneExpr.2025057731","url":null,"abstract":"<p><strong>Background: </strong>Cystic fibrosis (CF) is common genetic disorder in Europe and North America but rarer in Asian populations.</p><p><strong>Objective: </strong>To explore the clinical manifestations and gene mutations of cystic fibrosis.</p><p><strong>Methods: </strong>This case series study enrolled children with CF diagnosed in the pediatric respiratory department of Shandong Provincial Hospital affiliated to Shandong First Medical University between June 2016 and August 2022.</p><p><strong>Results: </strong>Seven children, including 6 girls and 1 boy, were enrolled. All 7 patients had recurrent wet cough and (chronic) pneumonia. Six patients suffered from chronic sinusitis, 4 patients had recurrent wheezing; 2 patients had chronic diarrhea, malnutrition and growth lag; 2 patients were complicated by allergic bronchopulmonary aspergillosis; and 1 patient had pancreatic insufficiency. Bronchiectasis, thickening of bronchial wall and mucous impaction, were seen in the chest CT of 7 children. Six patients showed a large amount of viscous sputum adhered to the bronchial wall by bronchoscopy. Infection of Pseudomonas aeruginosa was found in 6 cases, Staphylococcus aureus in 2 cases, and Aspergillus fumigatus in 2 cases by bronchoalveolar lavage fluid or sputum culture. Sweat sodium chloride test was performed in 3 cases, and the result showed that Cl-> 60 mmol/L. CFTR gene mutations were found in 7 cases, which were rare mutations of Caucasians, including 2 cases with new mutation sites (c.325T>G and 326A>G).</p><p><strong>Conclusions: </strong>The major clinical presentations of CF could be chronic and recurrent upper and lower respiratory tract infections, malnutrition, and digestive tract diseases. The rare and even new mutations of Caucasians on CFTR gene may occur in Chinese children.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 4","pages":"55-64"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144000448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cancer Network Macromolecules.","authors":"George L Eliceiri","doi":"10.1615/CritRevEukaryotGeneExpr.2025055921","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2025055921","url":null,"abstract":"<p><p>The members of the network (interactome) that controls cancer needs to be known. This network consists of proteins and non-coding, single-stranded RNAs, such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and transfer RNAs (tRNAs). miRNAs are 21-23 nucleotides-long, and degrade messenger RNAs (mRNAs) and lncRNAs. lncRNAs are longer than 200 nucleotides, and sponge (sequester) miRNAs.</p>","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":"35 3","pages":"75-84"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143451131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}