Similar Datasets
Project description:Purpose: To comprehensively profile the landscape of the mRNA N6-methyladenosine (m6A) modification in human colorectal cancer (CRC). Methylated RNA immunoprecipitation sequencing (MeRIP-seq) was explored to compare the difference in mRNA N6-methyladenosine (m6A) methylation between CRC tissues and adjacent normal control (NC) tissue. RNA-sequencing (RNA-seq) was performed to transcribe differentially expressed mRNAs. Conjoint analysis of MeRIP-seq and RNA-seq data was conducted to predict RNA-binding proteins (RBPs). Results: MeRIP-seq identified 1110 differentially m6A methylated sites (DMMSs) and 980 differentially m6A methylated genes (DMMGs) in CRC, with 50.13% of all modified genes showing unique m6A-modified peaks in CRC. RNA-seq showed 915 upregulated genes and 1463 downregulated genes in CRC. QRT-PCR verified the RNA-seq results by detecting the expression of some mRNAs. Conjoint analysis of MeRIP-seq and RNA-seq identified 400 differentially m6A methylated and expressed genes (DEGs), and pathway analysis detected that DMMGs and DEGs were closely related to cancer. After analyzing these DMMGs and DEGs through the GEPIA database, we found that the expression of B3GNT6, DKC1, SRPK1 and RIMKLB were associated with prognosis, and the expression of B3GNT6 and RIMKLB were associated with clinical stage. 17 RBPs were identified based on the DMMGs and DEGs, among which FXR1, FXR2, FMR1, IGF2BP2, IGF2BP3 and SRSF1 were obviously highly expressed in CRC, and FMR1, IGF2BP2 and IGF2BP3 were closely related to methylation, and might be involved in the development of CRC. Conclusions: This study comprehensively profiled m6A modification of mRNAs in CRC, which revealed possible mechanisms of m6A-mediated gene expression regulation.
2022-02-02 | GSE190388 | GEO
Project description:Identify m6A modified residues by m6A-irCLIP in polyA selected RNA from mouse CD4+ T cells
2018-02-14 | GSE107055 | GEO
Project description:Wilms tumor (WT), also known as nephroblastoma, is the most commonly observed renal tumor within the genitourinary tract of children and constitutes 5% of all childhood malignancies. In this study, we used microarray technology to explore methylation patterns in both WT and adjacent healthy tissues from excised kidneys prior to any chemotherapy treatment in stage I and II WTs. We report several differentially methylated regions that show potential as prognostic biomarkers for disease relapse, and overall patient survival. To explain the mechanistic role of DNA methylation changes in WT relapse, we explore the genes controlled by the differentially methylated IGF2 region, and show elevated expression of INS-IGF2 transcript in tumour tissue of patients that have relapsed after treatment. Altogether, this study provides insights into causes of chemotherapy resistance in patients with low risk WT.
2024-11-28 | GSE269241 | GEO
Project description:Purpose: Evaluation of the m6A modification of EBV and BJAB transcripts during EBV infection Methods: Human B lymphoma cell line BJAB was uninfected or infected with EBV for 24 hours. Total RNA from each sample were extracted. Intact mRNA was isolated from total RNA samples and then chemically fragmented to 100-nucleoside-long fragments. m6A methylated mRNAs were immunoprecipitated with anti-N6-methyadenosine (m6A) antibody (a part of the fragmented mRNAs was kept as input). Both m6A enriched mRNAs and input mRNAs were concentrated for RNA-seq library construction. Sequencing was performed using an Illumina HiSeq 4000. Results: EBV EBNA2 and BHRF1 transcripts were m6A modified and m6A modification of BJAB transcripts changed during EBV infection. Conclusions: Our study found that some EBV transcripts were m6A modified during EBV infection and EBV infection changed m6A modification profiles of BJAB transcripts.
2021-07-10 | GSE133936 | GEO
Project description:As the crucial m6A reader, YTHDF2 usually degrades the target mRNAs by recognizing the m6A modified sites, consequently altering m6A levels of each mRNA. In this study, we used m6A MeRIP sequencing to detect the m6A modification alterations in prostate cancer (PCa) cell line after knocking down YTHDF2 and identify how YTHDF2 promote the PCa progression by mediating the mRNA degradation in m6A-dependent way.
2020-11-09 | GSE129408 | GEO
Project description:Genome wide DNA methylation profiling of tumor adjacent normal tissue from patients with invasive breast cancer, as well as tissue from women undergoing reduction mammoplasty or prophylactic surgery. The Illumina Infinium 450k Human DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 485,577 CpGs in snap frozen breast tissue. Samples included 70 tumor-adjacent normal breast tissue with invasive disease, 8 tissues from breast prophylactic patients, and 18 tissues from breast reduction patients.
2015-04-15 | GSE67919 | GEO
Project description:Genome wide DNA methylation profiling of normal kidney (n=36), nephrogenic rest (n=22) and Wilms tumour (n=37) was performed using the Illumina 450k array. Two papers were composed after analysis of this data (1) describes comparative analysis of 22 matched normal kidney-Wilms tumour pairs which identified biomarker differentially methylated regions (DMRs) that could be detected in patient blood; (2) describes comparative analysis of 20 matched trios which identified changes in methylation associated with progression from the precursor lesion towards tumourigenesis.
2014-07-08 | GSE59157 | GEO
Project description:Beckwith-Wiedemann syndrome (BWS) is an overgrowth syndrome caused by a variety of molecular changes on chromosome 11p15.5. Children with BWS have a significant risk of developing Wilms tumours with the degree of risk being dependent on the underlying molecular mechanism. In particular, only a relatively small number of children with loss of methylation at the centromeric imprinting centre (IC2) were reported to have developed Wilms tumour. Discontinuation of tumour surveillance for children with BWS and loss of methylation at IC2 has been proposed in several recent publications. We report here three children with BWS reported to have loss of methylation at IC2 on clinical testing who developed Wilms tumour or precursor lesions. Using multiple molecular approaches and multiple tissues, we reclassified one of these cases to paternal uniparental disomy for chromosome 11p15.5. These cases highlight the current challenges in definitively assigning tumour risk based on molecular classification in BWS. The confirmed cases of loss of methylation at IC2 also suggest that the risk of Wilms tumour in this population is not low as previously thought. Therefore, we recommend that for now, all children with a clinical diagnosis of BWS be screened for Wilms tumour by abdominal ultrasonography until the age of 8 regardless of the molecular classification.
2017-03-01 | GSE95486 | GEO
Project description:To search for novel m6A-modified transcripts that are involved in the genesis of neuropathic pain, We collected the ipsilateral spinal cord at 7 days after chronic constriction injury and performed m6A peak profiling using MeRIP-seq
2021-03-29 | GSE171004 | GEO
Project description:The lack of model systems limits the preclinical testing of novel therapies to address Wilms tumor patient groups with poor outcomes. Therefore, we established 45 heterotopic Wilms tumor patient-derived xenografts (WTPDX) in CB17 scid-/- mice that capture the biological heterogeneity of Wilms tumor (WT). These WTPDX include six showing diffuse anaplasia, nine from patients who went on to experience disease relapse, and thirteen from patients with bilateral disease. WTPDX retained the genetic alterations and the global transcriptomic and methylation profile of corresponding primary WT. In addition, favorable histology WTPDX were chemosensitive, while unfavorable histology WTPDX were resistant to conventional chemotherapy with vincristine, actinomycin-D, and doxorubicin. This WTPDX library is a unique scientific resource that retains the spectrum of biological heterogeneity present in WT and provides an essential tool for the testing of novel targeted therapies in the era of precision medicine.
2019-02-14 | GSE110697 | GEO