Similar Datasets
Project description:Bone cancer pain (BCP), in which the majority is caused by metastasis from other cancer sites, is the most common type of chronic cancer pain and is not fully understood. The role of posttranscriptional modification in the pathogenesis of bone cancer pain has not been reported. Thus, in the present study, we performed MeRIP-seq to explore changes in m6a modification of transcripts and to provide a landscape of dysregulated transcripts in the spinal cord of bone cancer pain.
2025-06-30 | GSE213587 | GEO
Project description:Bone cancer pain (BCP), in which the majority is caused by metastasis from other cancer sites, is the most common type of chronic cancer pain. Bone cancer pain is developed accompanied by changes of numerous genes expression, from peripheral to central nervous system, which may account for this dysfunctional nociceptive perception. Although the pivotal role of lncRNA in neuropathic pain are well acknowledged, the involvement of lncRNA in bone cancer pain development are remain to be clarified. Thus, in the present study we performed transcriptome sequencing to explore changes in expression profiles of lncRNA and mRNA to provide a landscape of dysregulated miRNA in spinal cord of bone cancer pain.
2022-08-10 | GSE200307 | GEO
Project description:Bone cancer pain (BCP), in which the majority is caused by metastasis from other cancer sites, is the most common type of chronic cancer pain. Bone cancer pain is developed accompanied by changes of numerous genes expression, from peripheral to central nervous system, which may account for this dysfunctional nociceptive perception. Although the pivotal role of lncRNA in neuropathic pain are well acknowledged, the involvement of lncRNA in bone cancer pain development are remain to be clarified. Thus, in the present study we performed transcriptome sequencing to explore changes in expression profiles of lncRNA and mRNA to provide a landscape of dysregulated lncRNA and mRNA in spinal cord of bone cancer pain.
2020-01-11 | GSE137326 | GEO
Project description:Objectives: This study aimed to identify a set of differentially expressed genes (DEGs) in dorsal root ganglions (DRGs) between bone cancer pain (BCP) and sham BCP rats using RNA-sequencing (RNA-Seq). Methods: We established a rat BCP model by implanting MRMT-1 cells into the bone marrow cavity of left tibia. RNA-Seq was used to screen related genes. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis and protein-protein interaction (PPI) network analysis were conducted to investigate the bioinformatics functions of DEGs and possible potential pathological mechanisms of BCP. Results: RNA-Seq of ipsilateral DRGs from model rats identified a total of 152 DEGs compared to sBCP rats. The expression changes of four randomly selected DEGs were verified by qPCR. Four significant signaling pathways have been found for BCP including MAPK signaling pathway, calcium signaling pathway, apelin signaling pathway and oxytocin signaling pathway. Cxcl13 in DRGs was identified as a key player in the BCP model by comparing with published datasets in classic pain models. A core set of genes contributed to BCP mechanism were sorted out by PPI network analysis. Conclusions: These altered mRNAs and signaling pathways might be potential therapeutic targets for BCP treatment, which can guide future research on the molecular mechanism of BCP.
2023-12-12 | GSE249443 | GEO
Project description:Screening and identification of transcriptomic expression profiles of mice with bone cancer pain
| PRJNA892616 | ENA
Project description:Background: The skeletal system ranks as the third most common site for cancer metastasis, often leading to pain with nociceptive and neuropathic features. PD-1-targeting therapeutic antibodies offer effective cancer treatment but can cause treatment-related acute pain. Understanding the mechanisms of this pain and identifying potential interventions is still a challenge. Methods: A murine model of bone cancer pain was established using Lewis lung carcinoma (LLC) cells, followed by intravenous administration of nivolumab, a human anti-PD-1 monoclonal antibody. Pain thresholds were measured, and micro-CT images of the skeletal system were obtained. High-throughput sequencing of the spinal cord/colon transcriptome during the acute phase of bone cancer pain and gut microbiota analysis were performed. Immunofluorescence staining and western blot experiments assessed spinal cord microglia activation and acute pain-associated molecules. Results: PD-1 inhibition with nivolumab protected against bone degradation initiated by LLC cell administration but consistently induced acute pain during nivolumab treatment. Spinal cord and colon transcriptomics revealed an immunopathological pattern during tumor progression and the acute pain phase, with notable changes in interleukin and S100 gene families. Gut microbiota analysis post-immunotherapy showed a decline in beneficial bacteria associated with SCFA production. Activation of spinal cord microglia and enhanced glycolytic metabolism were confirmed as key factors in inducing acute pain following immunotherapy. Conclusions: This study reveals that nivolumab induces acute pain by activating microglia and enhancing glycolytic metabolism in the treatment of bone cancer and uncovers connections between transcriptomic changes, gut microbiota, and acute pain following ICB treatment. It offers novel insights into the relationship between immune checkpoint blockade therapies and pain management.
2023-09-14 | GSE242789 | GEO
Project description:Molecular characterization of the individual neuron types existing in the primate dorsal root ganglion and the relation to model organisms used for studying somatosensation and pain is critical for understanding the cellular origin of chronic pain and for translational aspects of biomedical research. However, molecular insights into the primate dorsal root ganglion are missing and a systematic comparison of strategies for somatosensation between the mouse and primates is lacking. Here we classify non-human primate sensory neurons based on their transcriptome and identify neuronal types with heritability to chronic pain. We identify nine neuronal types and use machine learning to expose an overall cross-species conserved strategy and shared taxonomy for nociception, although with differences at individual gene level, highlighting the importance of incorporating primate knowledge for the successful translation of discoveries in rodent model organisms. Genomic loci implicated in chronic pain were mapped onto specific primate sensory neuron types to identify the cellular origin of chronic pain. The common-variant genome-wide association results for chronic pain point to the same cells at the same pain sites and concentrate on two different neuronal types between pain disorders, suggesting that causative cell types and molecular mechanisms are different between different pain conditions.
2021-03-11 | GSE148238 | GEO
Project description:Six different mouse pain models were studied: (1) tumour-injection model for bone cancer pain; (2) partial sciatic nerve ligation (PSL) for neuropathic pain; (3) mechanical joint loading for osteoarthritis pain; (4) oxaliplatin-induced painful neuropathy for chemotherapy-induced pain; (5) hyperalgesic priming model for chronic muscle pain; and (6) complete Freund’s adjuvant (CFA)-injection for inflammatory pain. Transcriptomic microarray analyses were performed using RNA isolated from dorsal root ganglia.
2018-06-11 | E-MTAB-6864 | biostudies-arrayexpress
Project description:Background: Synovial inflammation is associated with pain severity in patients with knee osteoarthritis (OA). The aim here was to determine in a population with knee OA, whether synovial tissue from areas associated with pain exhibited different synovial fibroblast transcriptomes, compared to synovial tissue from sites not associated with pain. A further aim was to compare differences between early and end-stage disease synovial fibroblasts. Methods: Patients with early knee OA (n=29) and end-stage knee OA (n=22) were recruited. Patient reported pain was recorded by questionnaire and using an anatomical knee pain map. Proton density fat suppressed MRI axial and sagittal sequences were analysed and scored for synovitis. Synovial tissue was obtained from the medial and lateral parapatellar and suprapatellar sites. RNA sequencing was performed using Illumina’s NextSeq 500 and analysed with Galaxy web platform, usegalaxy.org, and Qlucore software. Transcriptomes were functionally characterised using Ingenuity Pathway Analysis. Findings: Parapatellar synovitis was significantly associated with increased OA pain perception. Functional pathway analysis revealed that early OA painful sites mediate immune cell recruitment and promote the formation and development of neurites. Conclusion: OA disease progression and the presence of pain in early OA is associated with different synovial pathotypes. Further interrogation of these pathotypes will increase our understanding of the role of synovitis in OA joint pain and provide a rationale for the therapeutic targeting to alleviate pain in patients.
2021-10-20 | GSE176223 | GEO
Project description:To evaluate ac4C acetylation in the spinal dorsal horn of rats with bone cancer pain.
2023-05-23 | GSE225571 | GEO