Causal relationships between skin microbiome and pathological scars: a bidirectional mendelian randomization study.

Skin bacteria infection could be a potential risk factor on wound scar formation, yet the specifics of this relationship are not fully understood. This research investigates the causal relationships between specific skin microbiome and these diseases by using bidirectional Mendelian randomization (MR). This study employed a bidirectional MR analysis using genome-wide association study (GWAS) data to analyze the associations between skin microbiome and pathological scar.

Mechanism of lncRNA FOXD3-AS1/miR-338-3p in the malignant progression of nasopharyngeal carcinoma through ceRNA.

This work aimed to analyze the impact of lncRNA FOXD3-AS1 (F-A) on the regulation of miR-338-3p (M) on the proliferation (Pro), migration (Mig), and invasion (Inv) of nasopharyngeal carcinoma (NPC) cells. F-A and M levels in human normal nasopharyngeal (NNP) NP69 cells and NPC CNE1 and CNE2 cells were detected by real-time quantitative PCR. After transfection or cotransfection with F-A shRNA, miR-338-3p mimic (MM), and miR-338-3p inhibitor (MI), cell Pro, Mig, and Inv (PMI) were detected using CCK-8, scratch healing, and Transwell chamber experiments, respectively.

CircSLC8A1 targets miR-181a-5p/HIF1AN pathway to inhibit the growth, migration and extracellular matrix deposition of human keloid fibroblasts.

Background: Circular RNAs (circRNAs) are identified as important regulators in human diseases, including keloid. The purpose of this study is to reveal the role and molecular mechanism of circSLC8A1 in keloid formation.

Methods: Expression of circSLC8A1, microRNA (miR)-181a-5p, and hypoxia inducible factor 1 alpha inhibitor (HIF1AN) were detected by quantitative real-time PCR.