Taking these findings together, our study revealed novel lncRNA signatures deregulated in UC and identified IFNG-AS1 as a novel regulator of IFNG inflammatory responses, suggesting the potential importance of noncoding RNA mechanisms on regulation of inflammatory bowel disease-related inflammatory responses.
Media from T-cells overexpressing IFNG-AS1 elicited an inflammatory signaling cascade in primary human peripheral blood mononuclear cells, suggesting the potential functional importance of IFNG-AS1 in IBD pathophysiology.
Taking these findings together, our study revealed novel lncRNA signatures deregulated in UC and identified IFNG-AS1 as a novel regulator of IFNG inflammatory responses, suggesting the potential importance of noncoding RNA mechanisms on regulation of inflammatory bowel disease-related inflammatory responses.
The present study provides evidences for participation of IFNG and IFNG-AS1 in the pathogenesis of breast cancer and warrants future studies to elaborate the underlying mechanism.
In this study, associations of lncRNA IFNG-AS1 expression with secretion of IFN-γ level in Sixty patients with brucellosis, which were divided into 3 groups (acute, chronic and relapse groups), as a case group were compared with 20 subjects with negative serological tests and brucellosis clinical manifestation as a control group.
The IBD associated long non-coding RNA IFNG-AS1 regulates the balance between inflammatory and anti-inflammatory cytokine production after T-cell stimulation.
We reanalyzed the nest-generation sequencing (NGS) gene panel testing results of patients who were diagnosed with FAP, but did not have APC mutations, at Yonsei Cancer Prevention Center between July 2016 and March 2018.
In the present study, we found that IFNG-AS1 expression was significantly higher in PA tissues than in nontumor tissues via qRT-PCR and RNA fluorescence in situ hybridization (FISH). shRNA-mediated IFNG-AS1 knockdown in HP75 cells significantly inhibited tumor progression, and IFNG-AS1 overexpression remarkably promoted tumor progression.
In conclusion, we speculated that TMEVPG1 could promote IFNG transcription, and IFNG over-expression negative feedback regulated on TMEVPG1 expression, which resulted in decreased TMEVPG1 in ITP patients.
Our results indicate that enhanced expression of lncRNA-IFNG-AS1 contributes to Th1 cell response in HT patients and may be involved in the pathogenesis of HT.
The present study provides evidences for participation of IFNG and IFNG-AS1 in the pathogenesis of breast cancer and warrants future studies to elaborate the underlying mechanism.
The results showed significant up-regulation of IFNG and down-regulation of IFNG-AS1 expression in children with ASD compared to controls (Fold change = 1.5, P < 0.0001; Fold change = -0.143, P = 0.013, respectively).