Abstract Objective The aim of this study was to evaluate the serum Syndecan-1 (SDC-1) levels in patients with immunoglobulin-A vasculitis (IgAV) in children and its relation with gastrointestinal involvements. Methods Sixty-eight children with IgAV and 48 healthy children were enrolled in this cross-sectional study. Clinical and related laboratory data were collected from a computerized hospital database. Serum SDC-1 was collected on admission prior to treatment. Results Forty-eight patients fully met the IgAV diagnostic criteria at admission (IgAV group), 20 patients with rash only and diagnosed IgAV during hospitalization (Purpura group). In IgAV group, 30 patients with gastrointestinal involvements (IgAV-GI group) and 18 patients without gastrointestinal involvements (IgAV-NGI group). SDC-1 serum levels were significantly higher in the IgAV group (86.37 ng/mL (IQR 59.16-117.14 ng/mL)) than in the controls (20.37 ng/mL (IQR 15.52-26.45 ng/mL)) and the Purpura group (32.66 ng/mL (IQR 14.87-49.89 ng/mL)). Additionally, SDC-1 (OR = 1.08) was independently associated with IgAV with a cut-off value (sensitivity and specificity) of 66.55 ng/mL (68.8%, 95.0%), and the area under the curve was 0.908. The serum SDC-1 levels of the IgAV-GI group (106.92 ± 50.12 ng/mL) were significantly higher than those in the IgAV-NGI group (67.52 ± 17.59 ng/mL). Logistic regression analysis showed that SDC-1 (OR = 1.03) was independently associated with IgAV-GI with a cut-off value of 89.39 ng/mL. Conclusions SDC-1 serum levels may mirror vascular endothelium injury and mucosal damage in IgAV. Its applicability as a surrogate biomarker in IgAV remains to be determined.

OBJECTIVE: The long non-coding RNA (lncRNA) KCNQ1 overlapping transcript 1 (KCNQ1OT1) exerts vital regulatory functions in diverse tumors. However, the biological function of KCNQ1OT1 in esophageal squamous cell carcinoma (ESCC) remains unclear. METHODS: KCNQ1OT1 expression was detected in ESCC tissues using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation, apoptosis, migration, and invasion were detected by the CCK-8 assay, EdU assay, flow cytometry analysis, and Transwell experiments, respectively. Bioinformatics analysis, luciferase reporter experiments, and RNA immunoprecipitation assays were used to predict and validate the regulatory relationships between KCNQ1OT1, microRNA-133b (miR-133b) and epidermal growth factor receptor (EGFR). RESULTS: KCNQ1OT1 expression was remarkably upregulated in ESCC tissues and cell lines. Overexpression of KCNQ1OT1 markedly promoted ESCC cell proliferation, migration, and invasion and enhanced the expression of N-cadherin, MMP-2, and MMP-9, but inhibited apoptosis and E-cadherin expression in ESCC cell lines; KCNQ1OT1 knockdown exerted the opposite effects. KCNQ1OT1 could directly bind to miR-133b and suppress its expression, and miR-133b reversed the effects of KCNQ1OT1 overexpression in ESCC cells. MiR-133b reduced the expression of epidermal growth factor receptor (EGFR); further, KCNQ1OT1 activated the phosphatidylinositol 3-kinase/AKT serine/threonine kinase 1 (PI3K/AKT) signaling pathway by repressing miR-133b repression and indirectly upregulating EGFR. KCNQ1OT1 expression was positively correlated with EGFR mRNA expression and negatively correlated with miR-133b expression. CONCLUSION: KCNQ1OT1 facilitates ESCC progression by sponging miR-133b and activating the EGFR/PI3K/AKT pathway.