To evaluate the short‐term and long‐term survival efficacy of an artificial liver support system (ALSS) in patients with acute‐on‐chronic liver failure (ACLF). A systematic search was performed for relevant published data in PubMed, Web of Science and Cochrane Library databases. Studies that evaluated the efficacy of ALSS in patients with ACLF and provided the short‐term or long‐term survival rate were included. A total of 10 studies involving 3685 patients were included in this analysis. The pooled 28‐day survival rate and 90‐day survival rate were 68.7% (95% CI: 64.5%–72.9%) and 53.4% (95% CI: 45.5%–61.4%), respectively. The pooled estimates of the OR for the 28‐day and 90‐day survival rates between the ALSS group and the control group were 1.91 (95% CI: 1.21–3.04) and 1.41 (95% CI: 1.17–1.70), respectively. Subgroup analysis showed that patients treated with lower levels of TBIL and MELD scores had a higher 28‐day survival rate (χ2 = 15.75, p < 0.01; χ2 = 13.80, p < 0.01). The present meta‐analysis suggests that ALSS treatment could remarkably improve short‐term survival rates in HBV‐ACLF patients, which implies that treatment with ALSS may help to reduce high mortality. Further prospective randomized trials are needed to validate these findings.
Background Hepatocellular carcinoma (HCC), comprises of the major primary liver cancer, is one of the most lethal malignancies in the world [1]. Increasing evidence has demonstrated that chromobox protein homolog 3 (CBX3) functioned as an oncogene in different cancers. However, its expression profiles and biological functions in HCC remain exactly unknown. Methods Data of CBX3 expression in HCC acquired from TCGA and GEO databases were analyzed. The biological functions of CBX3 in HCC were examined by in vitro experiments. Bioinformatics analysis, qRT-PCR and western blot were performed to explpore the mechanism of CBX3 involved in HCC. Results CBX3 mRNA was upregulated in HCC tissues, and overexpression of CBX3 mRNA was negatively correlated with malignancies and poor prognosis in HCC patients. Knocking down of CBX3 induced slower growth, less migration and fewer invasions of the HCC cells in vitro. Moreover, bioinformatics analysis and experimental observation indicated that CBX3 expression was correlated with cell cycle regulation proteins of HCC cells. Finally, Starbase predicted that the miR-139 could directly target CBX3 in HCC; Confirmatory experiments verified that miR-139 overexpression attenuated the HCC cells proliferation and migration, which could be reversed by overexpressing CBX3 concurrently. Conclusion Our results concluded that miR-139/CBX3 axis may involve in the HCC development through regulating cell cycle progression and may be a promising target in the treatment of HCC.
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