Purpose: Postmenopausal osteoporosis (PMO) patients may suffer from chronic pain and increased fractures due to brittle bones that seriously affect their normal work and life. Exploring the pathogenesis of PMO can help clinicians construct individualized therapeutic targets.
Methods: Differentially expressed genes (DEGs) were identified by analyzing the microarray assays of monocytes from 20 PMO and 20 control samples. Weighted correlation network analysis (WGCNA) and gene set enrichment analysis (GAEA) were performed. Genes associated with PMO were identified in the Comparative Toxicogenomics Database (CTD). miRNAs associated with osteoporosis were found in miRNet, and target genes were predicted. Hub genes and functional pathways associated with PMO were also identified. miRNA-mRNA networks were constructed. The association between hub genes and PMO was analyzed in the CTD.
Results: A total of 1055 genes were up-regulated, and 694 genes were down-regulated in PMO samples (P<0.01). Five modules were identified by WGCNA. The blue module was significantly associated with PMO and selected for further analysis (P < 0.05). A total of 229 genes were significantly associated with PMO gene significance and module membership. Pathway variations were predominantly enriched in mRNA metabolic process, RNA splicing, Notch signaling pathway, apoptosis, cytokine-cytokine receptor interaction and so on. We identified 10 hub genes associated with PMO with different inference scores.
Conclusion: We identified genes, miRNAs, and pathways associated with PMO. These molecules may participate in the pathogenesis of PMO and serve as therapeutic targets.
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http://dx.doi.org/10.2147/IJGM.S336310 | DOI Listing |
BMC Res Notes
December 2024
Department of Biological and Biomedical Sciences, Aga Khan University, Karachi, Pakistan.
Introduction: DU145 and LNCaP are classic prostate cancer cell lines. Characterizing their baseline transcriptomics profiles (without any intervention) can offer insights into baseline genetic features and oncogenic pathways that should be considered while interpreting findings after various experimental interventions such as exogenous gene transfection or drug treatment.
Methods: LNCaP and DU145 cell lines were cultured under normal conditions, followed by RNA extraction, cDNA conversion, library preparation, and RNA sequencing using the Illumina NovaSeq platform.
Genome Biol
December 2024
State Key Laboratory of Protein and Plant Gene Research, School of Advanced Agricultural Sciences, Peking-Tsinghua Center for Life Sciences, Peking University, Beijing, 100871, China.
Background: Promoters serve as key elements in the regulation of gene transcription. In mammals, loop interactions between promoters and enhancers increase the complexity of the promoter-based regulatory networks. However, the identification of enhancer-promoter or promoter-related loops in Arabidopsis remains incomplete.
View Article and Find Full Text PDFAdv Sci (Weinh)
December 2024
State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory of Pathobiology Ministry of Education, China-Japan Union Hospital of Jilin University, Changchun, 130033, China.
In the post-large era, various COVID-19 sequelae are getting more and more attention to health problems. Although the mortality rate of the COVID-19 infection is now declining, it is often accompanied by new clinical sequelae with different symptoms such as fatigue after infection, loss of smell. The degree of age, gender, virus infection seems to be weakly correlated with clinical symptoms.
View Article and Find Full Text PDFClin Epigenetics
December 2024
Hereditary Cancer Group, ONCOBELL Program, Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, Spain.
Background: Lynch syndrome (LS), characterised by an increased risk for cancer, is mainly caused by germline pathogenic variants affecting a mismatch repair gene (MLH1, MSH2, MSH6, PMS2). Occasionally, LS may be caused by constitutional MLH1 epimutation (CME) characterised by soma-wide methylation of one allele of the MLH1 promoter. Most of these are "primary" epimutations, arising de novo without any apparent underlying cis-genetic cause, and are reversible between generations.
View Article and Find Full Text PDFBiol Direct
December 2024
Urology Unit, Department of Surgery, Tor Vergata University of Rome, Rome, Italy.
Background: Prostate cancer is the most common diagnosed tumor and the fifth cancer related death among men in Europe. Although several genetic alterations such as ERG-TMPRSS2 fusion, MYC amplification, PTEN deletion and mutations in p53 and BRCA2 genes play a key role in the pathogenesis of prostate cancer, specific gene alteration signature that could distinguish indolent from aggressive prostate cancer or may aid in patient stratification for prognosis and/or clinical management of patients with prostate cancer is still missing. Therefore, here, by a multi-omics approach we describe a prostate cancer carrying the fusion of TMPRSS2 with ERG gene and deletion of 16q chromosome arm.
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