The systemic immune-inflammation index at kasai portoenterostomy: related to clinical outcomes.

BACKGROUND: Systemic Immune-Inflammation Index (SII), known as an easy, economical and useful marker, correlates with the balance of inflammation and immune response. However, the usefulness of SII in biliary atresia (BA) remains unclear. Therefore, we evaluated the relationship of SII level and postoperative clinical outcomes of BA. METHODS: Retrospective review of 168 patients with BA was conducted with assessments of demographic information, histological findings, laboratory parameters, and clinical outcomes. The LASSO logistic regression analysis was established using the "glmnet" software package to explore the influencing factors related to native liver survival time. Numerical variables were dichotomized based on the receiver operating characteristic (ROC) curve and Youden index yielding the best performance of prediction. R software was used for statistical analysis. RESULTS: Overall, the 24 month native liver survival rate was 43.5% (73 cases) after Kasai portoenterostomy. LASSO logistic regression analysis show that preoperative malnutrition (OR = 0.032, 95%CI 0.001-0.424), gamma-glutamyltransferase (GGT, OR = 0.994, 95%CI 0.987-0.998), lymphocyte count (LY, OR = 2.426, 95%CI 1.467-4.604), SII (OR = 0.977, 95%CI 0.960-0.989), and liver fibrosis grading (LFG, reference: Grade 1, Grade 3, OR = 0.076, 95%CI 0.007-0.614) were the independent influencing factors for 24 month native liver survival. ROC curve analysis showed that the area under the curve of SII level (0.919) was larger than that of preoperative malnutrition (0.690), LFG (0.759), GGT (0.747), and Ly (0.773). A SII < 140.09 was found to be a significant marker in the prediction of 24-month native liver survival, with 90.41% sensitivity and 93.68% specificity. Furthermore, the rates of 24-month native liver survival (33.1% vs. 72.7%), jaundice clearance (46.8% vs. 75.0%), and good liver function recovery (46.8% vs. 65.9%) were lower in the SII ≥ 140.09 group than that in the SII < 140.09 group (all P < 0.05), but there was no difference in the occurrence of cholangitis (P > 0.05). CONCLUSION: Preoperative malnutrition, GGT, Ly, SII, and LFG were independent influencing factors for postoperative 24-month native liver survival of BA. The SII level, as a routine haematological marker, has better universality and simplicity and is related to clinical outcomes after Kasai portoenterostomy.

CircSETD3 (Hsa_circ_0000567) Suppresses Hepatoblastoma Pathogenesis via Targeting the miR-423-3p/Bcl-2-Interacting Mediator of Cell Death Axis.

Background: Up until now, the role of circSETD3 (Has_circ_0000567) in regulating cancer development has been reported in several tumors, but the role and regulatory mechanism of circSETD3 in hepatoblastoma (HB) remain unclear. Methods: The qPCR and western blotting were used to determine the mRNA and protein levels in the present study. Stability of circular RNA was detected by RNA digested experiments. The gain-of-function and rescue experiments were used to explore the function and mechanism of circSETD3 in HB. Cell counting kit-8, colony formation, transwell assay, and xenograft mice model were used to detect effects and regulatory mechanism of circSETD3/miR-423-3p/Bim axis on cell aggressive phenotype in vitro and in vivo. Results: Here, we identified that circSETD3 downregulated in both HB clinical tissues and cell lines, compared to that of normal tissues and cells. Further gain-of-function experiments validated that circSETD3 overexpression inhibited cell proliferation, viability, migration, epithelial-mesenchymal transition (EMT) and tumorigenesis, and induced cell apoptosis in HB cells. Next, we validated that miR-423-3p targeted both circSETD3 and 3' untranslated region (3'UTR) of Bim, and circSETD3 positively regulated Bim in HB cells through sponging miR-423-3p in a competing endogenous RNA (ceRNA)-dependent manner. Furthermore, through conducting reversal experiments, we evidenced that the inhibiting effects of circSETD3 overexpression on HB development were abrogated by upregulating miR-423-3p and downregulating Bim. Conclusion: Taken together, we evidenced that circSETD3 sponged miR-423-3p to upregulate Bim, resulting in the inhibition of HB development.