Head and neck squamous cell carcinoma (HNSCC) exhibits considerable variability in patient outcome. It has been reported that SOX2 plays a role in proliferation, tumor growth, drug resistance, and metastasis in a variety of cancer types. Additionally, SOX9 has been implicated in immune tolerance and treatment failures.
View Article and Find Full Text PDFN-methyladenosine (mA) methylation can be deposited on chromatin-associated RNAs (caRNAs) by the RNA methyltransferase complex (MTC) to regulate chromatin state and transcription. However, the mechanism by which MTC is recruited to distinct genomic loci remains elusive. Here we identify RBFOX2, a well-studied RNA-binding protein, as a chromatin factor that preferentially recognizes mA on caRNAs.
View Article and Find Full Text PDFFunctional characterization of pseudouridine (Ψ) in mammalian mRNA has been hampered by the lack of a quantitative method that maps Ψ in the whole transcriptome. We report bisulfite-induced deletion sequencing (BID-seq), which uses a bisulfite-mediated reaction to convert pseudouridine stoichiometrically into deletion upon reverse transcription without cytosine deamination. BID-seq enables detection of abundant Ψ sites with stoichiometry information in several human cell lines and 12 different mouse tissues using 10-20 ng input RNA.
View Article and Find Full Text PDFMethylation of adenosine at N1 position yields N-methyladenosine (mA), which is an epitranscriptomic modification that regulates mRNA metabolism. Recent studies showed that altered mA methylation promotes acute and chronic neurological diseases. We currently evaluated the effect of focal ischemia on cerebral mA methylome and its machinery.
View Article and Find Full Text PDFBackground: N6-methyladenosine (mA) modification of RNA influences fundamental aspects of RNA metabolism and mA dysregulation is implicated in various human diseases. In this study, we explored the potential role of RNA mA modification in the pathogenesis of Alzheimer disease (AD).
Methods: We investigated the mA modification and the expression of mA regulators in the brain tissues of AD patients and determined the impact and underlying mechanism of manipulated expression of mA levels on AD-related deficits both in vitro and in vivo.
Background: Aspirin desensitization followed by daily aspirin use is an effective treatment for aspirin-exacerbated respiratory disease (AERD).
Objective: To assess clinical features as well as genetic, immune, cytological and biochemical biomarkers that might predict a positive response to high-dose aspirin therapy in AERD.
Methods: We enrolled 34 AERD patients with severe asthma who underwent aspirin desensitization followed by 52-week aspirin treatment (650 mg/d).
Background: N6-methyladenosine (mA) modification is known to impact many aspects of RNA metabolism, including mRNA stability and translation, and is highly prevalent in the brain.
Results: We show that mA modification displays temporal and spatial dynamics during neurodevelopment and aging. Genes that are temporally differentially methylated are more prone to have mRNA expression changes and affect many pathways associated with nervous system development.
It has been previously established that hypoxia leads to tumor development, treatment resistance, and a poor prognosis. Under oxygen deprivation, hypoxia-inducible factors (HIFs) are stimulated to activate the genes necessary for tumor development in a low-oxygen environment. These genes encode regulators of angiogenesis, epithelial-mesenchymal transition, and cellular metabolism.
View Article and Find Full Text PDFBackground: To date, there has been no reliable in vitro test to either diagnose or differentiate nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD). The aim of the present study was to develop and validate an artificial neural network (ANN) for the prediction of N-ERD in patients with asthma.
Methods: This study used a prospective database of patients with N-ERD (n = 121) and aspirin-tolerant (n = 82) who underwent aspirin challenge from May 2014 to May 2018.
Background: Aspirin desensitization (AD) is an effective and safe therapeutic option for patients with nonsteroidal anti-inflammatory drugs (NSAIDs)-exacerbated respiratory disease (N-ERD). The mechanisms driving its beneficial effects remain poorly understood.
Objective: To investigate the effect of long-term AD on clinical, biochemical and radiological changes in N-ERD patients.