Comparative and Functional Genomics最新文献

{"title":"KYNU as a Biomarker of Tumor-Associated Macrophages and Correlates with Immunosuppressive Microenvironment and Poor Prognosis in Gastric Cancer","authors":"Kaiyu Shen,&nbsp;Binyu Chen,&nbsp;Liu Yang,&nbsp;Wencang Gao","doi":"10.1155/2023/4662480","DOIUrl":"10.1155/2023/4662480","url":null,"abstract":"<div>\u0000 <p><i>Background</i>. Kynureninase (KYNU) is a potential prognostic marker for various tumor types. However, no reports on the biological effects and prognostic value of KYNU in gastric cancer (GC) exist. <i>Methods</i>. GC-associated single-cell RNA sequencing and bulk RNA sequencing (bulk-seq) data were obtained from the Gene Expression Omnibus and The Cancer Genome Atlas databases, respectively. The differential expression of KYNU between GC and normal gastric tissues was first analyzed based on the bulk-seq data, followed by an exploration of the relationship between KYNU and various clinicopathological features. The Kaplan–Meier survival and Cox regression analyses were performed to determine the prognostic value of KYNU. The relationship between KYNU expression and immune cell infiltration and immune checkpoints was also explored. The biological function of KYNU was further examined at the single-cell level, and in vitro experiments were performed to examine the effect of KYNU on GC cell proliferation and invasion. <i>Results</i>. KYNU expression was significantly elevated in GC samples. Clinical features and survival analysis indicated that high KYNU expression was associated with poor clinical phenotypes and prognosis, whereas Cox analysis showed that KYNU was an independent risk factor for patients with GC. Notably, high expression of KYNU induced a poor immune microenvironment and contributed to the upregulation of immune checkpoints. KYNU-overexpressing macrophages drove GC progression through unique ligand-receptor pairs and transcription factors and were associated with adverse clinical phenotypes in GC. KYNU was overexpressed in GC cells in vitro, and KYNU knockout significantly inhibited GC cell proliferation and invasion. <i>Conclusion</i>. High KYNU expression promotes an adverse immune microenvironment and low survival rates in GC. KYNU and KYNU-related macrophages may serve as novel molecular targets in the treatment of GC.</p>\u0000 </div>","PeriodicalId":55239,"journal":{"name":"Comparative and Functional Genomics","volume":"2023 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10635752/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89718225","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":"Correlation between LSM1 Expression and Clinical Outcomes in Glioblastoma and Functional Mechanisms","authors":"Changcheng Cai,&nbsp;Xingyu Chen,&nbsp;Jimin He,&nbsp;Chengwei Xiang,&nbsp;Yinggang Liu,&nbsp;Ke Wu,&nbsp;Ke Luo","doi":"10.1155/2023/1543620","DOIUrl":"10.1155/2023/1543620","url":null,"abstract":"<div>\u0000 <p><i>Background</i>. Glioblastoma (GBM) is an aggressive form of brain tumor characterized by limited treatment options and a bleak prognosis. Although the role of Like-Sm 1 (LSM1), a component of the mRNA splicing machinery, has been studied in various cancers, its significance in GBM remains unclear. The purpose of this research was to investigate the expression of LSM1 and its role in driving GBM progression. <i>Methods</i>. We analyzed gene expression data obtained from TCGA and GTEx databases to compare the levels of LSM1 expression between GBM and normal brain tissues. To assess the impact of LSM1, we conducted experiments using U87 GBM cells, wherein we manipulated LSM1 expression through overexpression and knockdown techniques. These experiments allowed us to evaluate cellular behaviors such as proliferation and invasion. Additionally, we explored the correlation between LSM1 expression and immune cell infiltration in GBM. <i>Results</i>. Our analysis of TCGA and GTEx datasets revealed a significant upregulation of LSM1 expression in GBM compared to normal brain tissues. In our in vitro experiments using U87 cells, we observed that LSM1 overexpression promoted cell proliferation and invasion, while LSM1 knockdown exerted the opposite effects. Moreover, we discovered correlations between LSM1 expression and immune cell infiltration in GBM, specifically involving TFH cells, CD56bright cells, macrophages, and Th2 cells. <i>Conclusions</i>. The findings of this study demonstrate the upregulation of LSM1 in GBM and its contribution to tumor progression by enhancing cell proliferation, invasion, and influencing immune cell infiltration. Our research sheds light on the potential oncogenic role of LSM1 in GBM and suggests its viability as a therapeutic target for this aggressive brain tumor.</p>\u0000 </div>","PeriodicalId":55239,"journal":{"name":"Comparative and Functional Genomics","volume":"2023 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10635750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89718224","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":"The Potential Mechanism of Curcumin in Treating Oral Squamous Cell Carcinoma Based on Integrated Bioinformatic Analysis","authors":"Wu Siyuan,&nbsp;Lv Xiaozhi,&nbsp;Wu Jialin,&nbsp;Haigang Wei,&nbsp;Shiwei Liu,&nbsp;Chen Zou,&nbsp;Jing Song,&nbsp;Li Xia,&nbsp;Ai Yilong","doi":"10.1155/2023/8860321","DOIUrl":"10.1155/2023/8860321","url":null,"abstract":"<div>\u0000 <p><i>Aims</i>. This study explores the effects of curcumin as a therapeutic agent against oral squamous cell carcinoma (OSCC). <i>Methods</i>. We acquired the targets of curcumin from three digital databases, including the Comparative Toxicogenomics Database, Search Tool for Interactions of Chemicals, and SwissTargetPrediction. Then, we identified the differentially expressed genes (DEGs) and the weighted gene coexpression network analysis-based key modules using the expression profiles of GSE23558 to acquire the OSCC-related genes. Additionally, the GeneCards and Online Mendelian Inheritance in Man databases were also used to identify the OSCC-related genes. Finally, curcumin-OSCC interaction genes were obtained by overlapping curcumin targets and OSCC-related genes. The enrichment analysis was performed by the ClusterProfiler algorithm and Metascape, respectively. Then, a protein-protein interaction network was created, and the maximal clique centrality algorithm was used to identify the top 10 hub genes. Besides, we examined the expression levels of hub genes in OSCC using The Cancer Genome Atlas database. <i>Results</i>. 927 DEGs were identified, including 308 upregulated ones and 619 downregulated ones. The cluster one-step network construction function of the WGCNA algorithm recognized a soft-thresholding power of 6, and 9083 genes were acquired. 2591 OSCC-related genes were obtained by overlapping the GSE23558-identified genes and the OSCC-related genes from disease target bases. Finally, we identified 70 candidate drug-disease interaction genes by overlapping the disease-related genes with the curcumin target. The enrichment analysis suggested that response to oxidative stress, epithelial cell proliferation, and AGE/RAGE pathway might involve in the effect of curcumin on OSCC. The topologic study identified the ten hub genes, including <i>VEGFA</i>, <i>AKT1</i>, <i>TNF</i>, <i>HIF1A</i>, <i>EGFR</i>, <i>JUN</i>, <i>STAT3</i>, <i>MMP9</i>, <i>EGF</i>, and <i>MAPK3</i>. A significant difference was observed in VEGFA, AKT1, TNF, HIF1A, EGFR, MMP9, EGF, and MAPK3 expression levels between head and neck squamous cell carcinoma and the normal controls. However, no significant difference was observed in <i>JUN</i> (<i>P</i> = 0.14) and <i>STAT3</i> (<i>P</i> = 0.054). <i>Conclusion</i>. This study provided an overview and basis for the potential mechanism of curcumin against OSCC. The following experiments should be performed to further understand the effectiveness and safety of curcumin in treating OSCC.</p>\u0000 </div>","PeriodicalId":55239,"journal":{"name":"Comparative and Functional Genomics","volume":"2023 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10590272/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49690414","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":"Identification of a Novel Variant of PDGFC Associated with Nonsyndromic Cleft Lip and Palate in a Chinese Family","authors":"Xin Yu,&nbsp;Simin Yang,&nbsp;Wenqian Xia,&nbsp;Xiaorong Zhou,&nbsp;Meiqin Gao,&nbsp;Hui Shi,&nbsp;Yan Zhou","doi":"10.1155/2023/8814046","DOIUrl":"10.1155/2023/8814046","url":null,"abstract":"<div>\u0000 <p>Nonsyndromic cleft lip with or without cleft palate (NSCL/P) accounts for 70% of the total number of patients with cleft lip with or without cleft palate (CL/P) and is the most common type of congenital deformity of the craniomaxillofacial region. In this study, whole exome sequencing (WES) and Sanger sequencing were performed on affected members of a Han Chinese family, and a missense variant in the platelet-derived growth factor C (<i>PDGFC</i>) gene (NM_016205: c.G93T: p.Q31H) was identified to be associated with NSCL/P. Bioinformatic studies demonstrated that the amino acid corresponding to this variation is highly conserved in many mammals and leads to a glutamine-to-histidine substitution in an evolutionarily conserved DNA-binding domain. It was found that the expression of <i>PDGFC</i> was significantly decreased in the dental pulp stem cells (DPSCs) of NSCL/P cases, compared to the controls, and that the variant (NM_016205: c.G93T) reduced the expression of <i>PDGFC</i>. In addition, the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed that <i>Pdgfc</i> deficiency disrupted NSCL/P-related signaling pathways such as the MAPK signaling pathway and cell adhesion molecules. In conclusion, our study identified a missense variant (NM_016205: c.G93T) in exon 1 of <i>PDGFC</i> potentially associated with susceptibility to NSCL/P.</p>\u0000 </div>","PeriodicalId":55239,"journal":{"name":"Comparative and Functional Genomics","volume":"2023 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10539090/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41134330","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":"tRNA-Uridine Aminocarboxypropyltransferase DTW Domain Containing 2 Suppresses Colon Adenocarcinoma Progression","authors":"Yun Qian,&nbsp;Yu-Jiang Li,&nbsp;Yi-Wei Fu,&nbsp;Cui-Xia Liu,&nbsp;Juan Wang,&nbsp;Bin Yang","doi":"10.1155/2023/4354536","DOIUrl":"10.1155/2023/4354536","url":null,"abstract":"<div>\u0000 <p><i>Background</i>. DTW Domain Containing 2 (DTWD2) is a newly identified transfer RNA-uridine aminocarboxypropyltransferase. Dysregulated expression of DTWD1 has been reported in several malignancies, nevertheless, the role of DTWD2 in cancers remains completely unknown. Here, we aimed to initially investigate the expression and role of DTWD2 in colon adenocarcinoma. <i>Methods</i>. We first evaluated the transcription and mRNA levels of DTWD2 using data from The Cancer Genome Atlas. Besides, we tested its mRNA and protein expression in our enrolled retrospective cohort. Univariate and multivariate analyses were conducted to assess its prognostic value. Cellular experiments and xenografts were also performed to validate the role of DTWD2 in colon cancer progression. <i>Results</i>. DTWD2 was downregulated in colon adenocarcinoma and associated with poor prognosis. Lymph node metastasis, distant metastasis, and advanced tumor stage are all characterized by lower DTWD2 levels. Furthermore, Cox regression analysis demonstrated that DTWD2 is a novel independent prognostic factor for colon cancer patients. Finally, cellular and xenograft data demonstrated that silencing DTWD2 significantly enhanced colon cancer growth. <i>Conclusion</i>. Low expression of DTWD2 may be a potential molecular marker for poor prognosis in colon cancer.</p>\u0000 </div>","PeriodicalId":55239,"journal":{"name":"Comparative and Functional Genomics","volume":"2023 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10517874/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41128997","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":"An Analysis of the Gene Expression Associated with Lymph Node Metastasis in Colorectal Cancer","authors":"Hongjie Yang,&nbsp;Jiafei Liu,&nbsp;Peishi Jiang,&nbsp;Peng Li,&nbsp;Yuanda Zhou,&nbsp;Zhichun Zhang,&nbsp;Qingsheng Zeng,&nbsp;Min Wang,&nbsp;Luciena Xiao Xiao,&nbsp;Xipeng Zhang,&nbsp;Yi Sun,&nbsp;Siwei Zhu","doi":"10.1155/2023/9942663","DOIUrl":"10.1155/2023/9942663","url":null,"abstract":"<div>\u0000 <p><i>Objective</i>. This study aimed to explore the genes regulating lymph node metastasis in colorectal cancer (CRC) and to clarify their relationship with tumor immune cell infiltration and patient prognoses. <i>Methods.</i> The data sets of CRC patients were collected through the Cancer Gene Atlas database; the differentially expressed genes (DEGs) associated with CRC lymph node metastasis were screened; a protein–protein interaction (PPI) network was constructed; the top 20 hub genes were selected; the Gene Ontology functions and the Kyoto Encyclopedia of Genes and Genomes pathways were enriched and analyzed. The Least Absolute Shrinkage and Selection Operator (LASSO) regression method was employed to further screen the characteristic genes associated with CRC lymph node metastasis in 20 hub genes, exploring the correlation between the characteristic genes and immune cell infiltration, conducting a univariate COX analysis on the characteristic genes, obtaining survival-related genes, constructing a risk score formula, conducting a Kaplan–Meier analysis based on the risk score formula, and performing a multivariate COX regression analysis on the clinical factors and risk scores. <i>Results</i>. A total of 62 DEGs associated with CRC lymph node metastasis were obtained. Among the 20 hub genes identified via PPI, only calcium-activated chloride channel regulator 1 (CLCA1) expression was down-regulated in lymph node metastasis, and the rest were up-regulated. A total of nine characteristic genes associated with CRC lymph node metastasis (KIF1A, TMEM59L, CLCA1, COL9A3, GDF5, TUBB2B, STMN2, FOXN1, and SCN5A) were screened using the LASSO regression method. The nine characteristic genes were significantly related to different kinds of immune cell infiltration, from which three survival-related genes (TMEM59L, CLCA1, and TUBB2B) were screened. A multi-factor COX regression showed that the risk scores obtained from TMEM59L, CLCA1, and TUBB2B were independent prognostic factors. Immunohistochemical validation was performed in tissue samples from patients with rectal and colon cancer. <i>Conclusion</i>. TMEM59L, CLCA1, and TUBB2B were independent prognostic factors associated with lymphatic metastasis of CRC.</p>\u0000 </div>","PeriodicalId":55239,"journal":{"name":"Comparative and Functional Genomics","volume":"2023 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10501847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10672031","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":"Identification of Potential Abnormal Methylation-Modified Genes in Coronary Artery Ectasia","authors":"Xiuchun Yang,&nbsp;Yijun Zong,&nbsp;Zhentian Zhang,&nbsp;Yan Zhao,&nbsp;Xueying Gao,&nbsp;Jie Zhang,&nbsp;Qian Hou,&nbsp;Renyi Li,&nbsp;Bing Xiao","doi":"10.1155/2023/4969605","DOIUrl":"10.1155/2023/4969605","url":null,"abstract":"<div>\u0000 <p><i>Background</i>. Coronary artery ectasia (CAE) is an easily recognized abnormality of coronary artery anatomy and morphology. However, its pathogenesis remains unclear. <i>Objectives</i>. This study aimed to identify abnormal methylation-modified genes in patients with CAE, which could provide a research basis for CAE. <i>Methods</i>. Peripheral venous blood samples from patients with CAE were collected for RNA sequencing to identify differentially expressed genes (DEGs), followed by functional enrichment. Then, the DNA methylation profile of CAE was downloaded from GSE87016 (HumanMethylation450 BeadChip data, involving 11 cases and 12 normal controls) to identify differentially methylated genes (DMGs). Finally, after taking interaction genes between DEGs and DMGs, abnormal methylation-modified genes were identified, followed by protein–protein interaction analysis and expression validation using reverse transcriptase polymerase chain reaction. <i>Results</i>. A total of 152 DEGs and 4318 DMGs were obtained from RNA sequencing and the GSE87016 dataset, respectively. After taking interaction genes, 9 down-regulated DEGs due to hypermethylation and 11 up-regulated DEGs due to hypomethylation were identified in CAE. A total of 10 core abnormal methylation-modified genes were identified, including six down-regulated DEGs due to hypermethylation (netrin G1, ADAM metallopeptidase domain 12, immunoglobulin superfamily member 10, sarcoglycan dela, Dickkopf WNT signaling pathway inhibitor 3, and GATA binding protein 6), and four up-regulated DEGs due to hypomethylation (adrenomedullin, ubiquitin specific peptidase 18, lymphocyte antigen 6 family member E, and MX dynamin-like GTPase 1). Some signaling pathways were identified in patients with CAE, including cell adhesion molecule, O-glycan biosynthesis, and the renin–angiotensin system. <i>Conclusions</i>. Abnormal methylation-modified DEGs involved in signaling pathways may be involved in CAE development.</p>\u0000 </div>","PeriodicalId":55239,"journal":{"name":"Comparative and Functional Genomics","volume":"2023 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10474963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10152706","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":"Stratifin Promotes Hepatocellular Carcinoma Progression by Modulating the Wnt/β-Catenin Pathway","authors":"Shan-Ping Ye,&nbsp;Hong-Xin Yu,&nbsp;Wei-Jie Lu,&nbsp;Jun-Fu Wang,&nbsp;Tai-Yuan Li,&nbsp;Jun Shi,&nbsp;Xiao-Ye Cheng","doi":"10.1155/2023/9731675","DOIUrl":"10.1155/2023/9731675","url":null,"abstract":"<div>\u0000 <p>Abnormal stratifin (SFN) expression is closely related to the progression of several human cancers, but the potential roles of SFN in hepatocellular carcinoma (HCC) remain largely unknown. In this study, we found that SFN was upregulated in HCC cell lines and tissues and was positively associated with tumor size, poor differentiation, Tumor Node Metastasis (TNM) stage, and vascular invasion. In addition, high expression levels of SFN were associated with poor overall survival and disease-free survival. Biologically, downregulation of SFN suppressed tumor cell proliferation, epithelial–mesenchymal transition (EMT), invasion, and migration in vitro and tumor growth in vivo. However, overexpression of SFN promoted cell proliferation, EMT, invasion, and migration in vitro and tumor growth in vivo. Mechanistically, overexpression of SFN activated the Wnt/<i>β</i>-catenin pathway by promoting Glycogen synthase kinase-3 beta (GSK-3<i>β</i>) phosphorylation, decreasing <i>β</i>-catenin phosphorylation, promoting <i>β</i>-catenin transport into the nucleus, and enhancing the expression of c-Myc, whereas depletion of SFN inhibited the Wnt/<i>β</i>-catenin pathway. In addition, TOPFlash/FOPFlash reporter assays showed that overexpression or downregulation of SFN obviously increased or decreased, respectively, the activity of the Wnt/<i>β</i>-catenin pathway. Our results indicated that SFN plays an important role in HCC, possibly providing a prognostic factor and therapeutic target for HCC.</p>\u0000 </div>","PeriodicalId":55239,"journal":{"name":"Comparative and Functional Genomics","volume":"2023 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10427227/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10017140","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":"circ_0008285 Regulates Glioma Progression via the miR-384/HMGB1 Axis","authors":"Manli Yan,&nbsp;Caihong Hu,&nbsp;Qi Hu,&nbsp;Heran Ma,&nbsp;Changjiang Lei,&nbsp;Yamei Liu","doi":"10.1155/2023/1680634","DOIUrl":"10.1155/2023/1680634","url":null,"abstract":"<div>\u0000 <p><i>Background</i>. Recent studies indicate that circular RNAs (circRNAs) have been implicated in the initiation or progression of a wide spectrum of diseases. In the current study, we explored the potential engagement of circ_0008285 in glioma and investigated the downstream regulators. <i>Methods.</i> The detection of circ_0008285 level in glioma specimens and cell lines was conducted by quantitative real-time polymerase chain reaction. The chi-squared test was employed to evaluate the relationship between the circ_0008285 level and the clinical features of glioma patients. The roles of circ_0008285 on the proliferation and apoptosis of glioma cells were studied by knockdown experiment. Meanwhile, the regulatory relationship of circ_0008285, miR-384, and high mobility group protein B1 (HMGB1) was explored in glioma cells, and we explored the effects of circ_0008285/miR-384/HMGB1 pathway on glioma cells. <i>Results</i>. In glioma specimens and cell lines, the expression of circ_0008285 was significantly increased, and a high circ_0008285 level was associated with a larger tumor size and more advanced grading in glioma patients. Furthermore, downregulating circ_0008285 suppressed proliferation and triggered apoptosis of glioma cells, which was associated with a cell cycle arrest at the G1/G0 phase. Mechanism studies indicated that circ_0008285 regulated HMGB1 by sponging miR-384. Functional experiments demonstrated that circ_0008285 promoted the malignant phenotype of glioma cells by miR-384/HMGB1 axis. <i>Conclusion</i>. Our study revealed circ_0008285 as a novel oncogenic factor in glioma through modulating the miR-384/HMGB1 pathway, suggesting that targeting circ_0008285 could serve as a strategy for glioma management.</p>\u0000 </div>","PeriodicalId":55239,"journal":{"name":"Comparative and Functional Genomics","volume":"2023 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10415084/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10000995","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":"Genomic Regions and Candidate Genes Associated with Milk Production Traits in Holstein and Its Crossbred Cattle: A Review","authors":"R. Bekele,&nbsp;M. Taye,&nbsp;G. Abebe,&nbsp;S. Meseret","doi":"10.1155/2023/8497453","DOIUrl":"10.1155/2023/8497453","url":null,"abstract":"<div>\u0000 <p>Genome-wide association studies (GWAS) are a powerful tool for identifying genomic regions and causative genes associated with economically important traits in dairy cattle, particularly complex traits, such as milk production. This is possible due to advances in next-generation sequencing technology. This review summarized information on identified candidate genes and genomic regions associated with milk production traits in Holstein and its crossbreds from various regions of the world. Milk production traits are important in dairy cattle breeding programs because of their direct economic impact on the industry and their close relationship with nutritional requirements. GWAS has been used in a large number of studies to identify genomic regions and candidate genes associated with milk production traits in dairy cattle. Many genomic regions and candidate genes have already been identified in Holstein and its crossbreds. Genes and single nucleotide polymorphisms (SNPs) that significantly affect milk yield (MY) were found in all autosomal chromosomes except chromosomes 27 and 29. Half of the reported SNPs associated with fat yield and fat percentage were found on chromosome 14. However, a large number of significant SNPs for protein yield (PY) and protein percentage were found on chromosomes 1, 5, and 20. Approximately 155 SNPs with significant influence on multiple milk production traits have been identified. Several promising candidate genes, including diacylglycerol O-acyltransferase 1, plectin, Rho GTPase activating protein 39, protein phosphatase 1 regulatory subunit 16A, and sphingomyelin phosphodiesterase 5 were found to have pleiotropic effects on all five milk production traits. Thus, to improve milk production traits it is of practical relevance to focus on significant SNPs and pleiotropic genes frequently found to affect multiple milk production traits.</p>\u0000 </div>","PeriodicalId":55239,"journal":{"name":"Comparative and Functional Genomics","volume":"2023 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10400298/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9950629","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}