Hepatocellular Carcinoma (HCC) currently remains one of the most lethal malignancies worldwide. Recently, long non-coding RNAs (lncRNAs) had been demonstrated to play a crucial role in the progression of multiple human cancers, including HCC. In this study, we found that lncRNA DUXAP8 was upregulated in tumor samples and served as an oncogene in HCC. Bioinformatics analysis showed that DUXAP8 was significantly associated with the regulation of centrosome organization, homologous recombination, meiotic cell cycle process, sister chromatid segregation, nuclear chromosome segregation, and RNA export from the nucleus. The knockdown of DUXAP8 significantly suppresses cell proliferation and the cell cycle but induces cell apoptosis in HCC. Mechanically, the present study showed that DUXAP8 serves as a sponge of MiR-490-5p to promote the expression of BUB1 in HCC. Although the underlying regulatory mechanisms of DUXAP8 in HCC require further investigation, this study, for the first time, showed that DUXAP8 can serve as a new therapeutic target for HCC.

Preeclampsia (PE) is a pregnancy-specific syndrome that may be lifethreatening to pregnancies and fetus. Glutathione Peroxidase 4 (GPx4) is a powerful antioxidant enzyme that can provide protection from oxidative stress damage which plays a pivotal role in the pathology of PE. Therefore, this study aims to investigate the association between Gpx4 polymorphisms and the susceptibility to PE in Chinese Han women. TaqMan allelic discrimination real-time PCR was used to perform the genotyping of rs713041 and rs4807542 in 1008 PE patients and 1386 normotensive pregnancies. Obviously statistical difference of genotypic and allelic frequencies were found of rs713041 in GPx4 between PE patients and controls and the C allele has the higher risk for pathogenesis of PE (χ2 = 12.292, P = 0.002 by genotype; χ2 = 11.035, P = 0.001, OR = 1.216, 95% CI 1.084–1.365 by allele). Additionally, when subdividing these samples into CC + CT and TT groups, we found a significant difference between the two groups (χ2 = 11.241, P = 0.001, OR = 1.417, 95% CI 1.155–1.738). Furthermore, the genotype of rs713041 was found to be associated with the mild, severe and early-onset PE. Our results suggest that rs713041 in GPx4 may play a key role in the pathogenesis of PE.

The role of microRNA-124a (miR-124a) in the regulation of T cell activation and immunity in patients with AIDS, was studied to provide new insights for the study, diagnosis, alleviation and treatment of AIDS. RT-qPCR technique was used to quantitatively analyze the expression of miR-124a in peripheral blood CD4+ T cells. Dual-luciferase reporter assay system was established to report possible regulatory relations between miR-124a and its potential target gene SIRT1. RT-qPCR and western blot analysis were used to detect the expression level of mRNA and protein of the target genes in T cells. Normal CD4+ T cells from controls were transfected with miR-124a mimics and its negative control, and miR-124a inhibitor and its negative control were transfected into CD4+ T cells from patients with AIDS by T lymphocyte transfection kit to detect the relative expression level of SIRT1 mRNA and protein. The levels of interferon (IFN)-γ, interleukin (IL)-10, transforming growth factor (TGF)-β, IL-2, IL-4 and IL-6 secreted by T helper cells were detected by enzyme-linked immunosorbent assay (ELISA). miR-124a was upregulated in CD4+ T cells of patients with AIDS. The results of firefly luciferase activity detection showed that miR-124a can directly interact with target gene SIRT1 and negatively regulate its expression. miR-124a mimics/inhibitor transfection experiments showed that overexpression of miR-124a in normal CD4+ T cells significantly reduced SIRT1 expression compared with control group, and the expression of miR-124a was positively correlated with IL-10 and TGF-β expression and negatively correlated with IFN-γ expression, but showed no correlation with other cytokines. In AIDS patients, the inhibition of expression of miR-124a in CD4+ T cells significantly increased the expression of SIRT, at the same time, the expression levels of IL-10 and TGF-β were significantly decreased, while the expression level of IFN-γ was significantly increased and no significant difference was found in the expression of other cytokines. The expression of miR-124a in CD4+ T cells of AIDS patients was upregulated and the Th2 type CD4+ T cells are activated by SIRT1 expression inhibition, which in turn enhance the immunity of HIV-infected cells. Our study provides a new molecular target for the diagnosis, alleviation and treatment of AIDS.

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Our study retrospectively investigated the expression of forkhead/winged helix transcription factor (Foxp3) in renal tissue and clinical features of patients with hepatitis B virus (HBV)-associated glomerulonephritis (HBV-GN). A total of 58 patients with HBV-GN were assigned to group A; 45 serum and renal tissue HBsAg-negative patients with nephritis were group B; 24 serum HBsAg-positive and renal tissue HBsAg-negative patients with slightly increased serum creatinine without nephritis were group C. Clinical manifestations, laboratory indices and renal biopsies were recorded. Expression of Foxp3, CD4 and CD25 in renal tissue was detected by immunohistochemistry. In group A, 74.1% were serum HBeAg-negative, with serum complement C3 level of 0.99±0.27 g/l, and deposition rates of renal complement C3 and C1q in renal tissue of 34.9 and 16.3% respectively; 25.9% were serum HBeAg-positive, with serum complement C3 level of 0.19±0.17 g/l, and deposition rates of renal complement C3 and C1q in renal tissue of 80 and 46.7%, respectively. A significant difference was found in C3 and C1q between HBeAg-negative and HBeAg-positive group (P<0.05). Increased urinary protein and decreased serum albumin were found in patients in group A with moderate levels of HBV DNA compared with patients with low levels of HBV DNA in the same group over 24 h (P<0.05). The numbers of Foxp3+ lymphocytes, CD4+ T cells and CD25+ T cells in the tubulointerstitium of patients in groups A and B were 3.41±1.16 vs. 3.52±1.27, 2.78±0.15 vs. 3.12±0.17 and 2.90±0.20 vs. 3.09±0.18, respectively. The clinical manifestation of HBV-GN is nephrotic syndrome, and HBV DNA is correlated with urinary protein and serum albumin levels. Activation of C3 and C1q may be related to the pathogenesis of HBV-GN in serum HBeAg-positive patients. Downregulation of Foxp3 expression in regulatory T cells is related to the development and progression of HBV-GN.