Purpose: To build a microRNA and gene signature of severe cutaneous adverse drug reactions (SCAR), including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN
Background
Sepsis reaction is a response to an infection composed of genetic elements. This research aims to better understand how sepsis affects the molecular pathways in whole blood samples.
Methods
Whole blood samples from healthy controls (n = 18), sepsis nonsurvivors (n = 9), and sepsis survivors (n = 26) were retrieved from the gene expression omnibus (GEO) collection of the national center for biotechnology information (NCBI) (accession number GSE54514). The NCBI's GEO2R program was used to determine differential expression, and the ingenuity pathway analysis (IPA) software was utilized to do a pathway analysis.
Results
In sepsis patients, 2672 genes were substantially differently expressed (p value 0.05). One thousand three hundred four genes were overexpressed, and one thousand three hundred sixty-eight were under-expressed. The inhibition of ARE-mediated mRNA degradation pathway and the Pl3K/AKT signaling spliceosomal cycle were the most significant canonical pathways identified by ingenuity pathway analysis (IPA). The IPA upstream analysis predicted the ESR1, SIRT1, and PTPRR proteins, and the drugs filgrastim and fluticasone were top transcriptional regulators.
Conclusions
The inhibition of ARE-mediated mRNA degradation pathway and the Pl3K/AKT signaling spliceosomal cycle were highlighted as essential pathways of inflammation by IPA, indicating widespread cancer owing to sepsis. Our data imply that sepsis considerably influences gene pathways in whole blood samples, pointing to possible targets for sepsis treatment.
Background: Colorectal cancer (CRC) is currently the third most common cancer type in males and the second most occurring in females. The role of microRNA (miRNA) in the development of colorectal cancer is not fully elucidated. Therefore, understanding the mechanistic interaction between miRNA and their target oncogenes may hold great importance as a possible target for interventional anticancer therapy.
Aims: To identify miRNAs that are part of the regulating pathway of Monocarboxylate Transporter-4 (MCT4) and Vascular Endothelial Growth Factor (VEGF) oncogenes.
Study Design: We used publicly available prediction tools (e.g. TargetScan, MicroCosm, PicTar, and DIANA-microT-CDS) to identify the possible miRNA that target the two oncogenes.
Methodology: We used the GeneMania database to visualize the network and verify gene names and remove ambiguity and duplications. Furthermore, we used miRTarBase database to identify experimentally validated targets which we used to further confirm miRNA-oncogene relationships. Finally, we utilized miR-Mfold web-tool to further visualize the circular structures and the simulated miR-1 and miR-206 targeting arrangements.
Results: We found two putative miRNA (miR-1 and miR-206) that may downregulate MCT4 coded by SLC16A3 gene and VEGF which is coded by VEGF gene. We found relationships between the validated target genes of miR-1 and miR-206 through GeneMania which we extracted from the literature. And we elucidated the proposed structure of these two miRNAs through miR-Mfold web-tool.
Conclusion: Our results elucidated a novel regulation pathway in CRC cells and may suggest a potential therapeutic approach for CRC therapy. MiR-1 and miR-206 may help cells go to apoptosis and inhibit the angiogenesis of colorectal cancer cells by down-regulation of MCT4 and VEGF proteins in tumor tissues.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.