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Both NNT‑AS1 and SOX4 knockdown inhibited GC cell proliferation, migration and invasion, and enhanced GC cell apoptosis. Moreover, the results indicated that NNT‑AS1 modulated SOX4 expression by sponging miR‑142‑5p. In addition, SOX4 overexpression reversed NNT‑AS1 knockdown‑mediated effects on GC cell proliferation, apoptosis, migration and invasion. NNT‑AS1 knockdown blocked the Wnt/β‑catenin signaling pathway via the miR‑142‑5p/SOX4 axis. Collectively, the present study indicated that NNT‑AS1 knockdown decreased GC cell proliferation, migration and invasion, and induced GC cell apoptosis by regulating the miR‑142‑5p/SOX4/Wnt/β‑catenin signaling pathway axis.Tumor angiogenesis is a hallmark of liver cancer and is necessary for tumor growth and progression. Supervillin (SVIL) is highly expressed and implicated in several malignant processes of liver cancer. However, the functional relationships between SVIL and tumor angiogenesis in liver cancer have not yet been fully elucidated. The present study was based on bioinformatics analysis, patient tissue sample detection, three‑dimensional simulated blood vessel formation, a series of cytological experiments and mouse models. The results demonstrated the important role of SVIL in the progression of malignant liver cancer and tumor angiogenesis, both in terms of vasculogenic mimicry (VM) and endothelium‑dependent vessel (EDV) development. SVIL knockdown inhibited VM formation and induced tumor cell apoptosis via the VEGF‑p38 signaling axis and through various VM‑associated transcriptional factors, including vascular endothelial‑cadherin, matrix metalloproteinase 9/12 and migration‑inducing protein 7. SVIL may therefore be considered a potential tumor vascular biomarker and a promising therapeutic target for patients with liver cancer.Increasing evidence suggests that long non-coding RNAs (lncRNAs) serve a crucial role in predicting prognosis for hepatocellular carcinoma (HCC). However, prognostic performance may not be the same for alcohol‑related HCC. The aim of the present study was to screen prognosis‑associated lncRNAs and construct a risk scoring system for alcohol‑related HCC. The expression profiles of lncRNAs in 113 patients with alcohol‑related HCC and 224 with non‑alcohol‑related HCC were obtained from The Cancer Genome Atlas (TCGA) database and screened for differentially expressed lncRNAs. Cox regression analysis was performed to identify prognosis‑associated lncRNAs and select the optimal lncRNA model. A risk scoring system was established to calculate the risk score for each patient. The prognostic ability of this system was tested. Functional enrichment analysis was performed for genes that were highly associated with lncRNA expression. A total of 102 differentially expressed lncRNAs were identified between alcohol‑related and non‑alcohol‑related HCC. Four lncRNAs (AC012640.1, AC013451.2, AC062004.1 and LINC02334) were used to construct the risk assessment model to predict overall survival (OS), and five lncRNAs (ERVH48‑1, LINC02043, LINC01605, AC062004.1 and AL139385) were used to predict recurrence‑free survival (RFS). Patients were assigned to high‑ or low‑risk groups according to the risk score. OS in the high‑risk group was significantly shorter than that of the low‑risk group. The area under the receiver operating characteristic (ROC) curve of risk scoring systems was >0.7. click here The risk score was an independent prognostic factor for alcohol‑related HCC. Functional enrichment analysis demonstrated that lncRNA‑related genes found in this system were mainly involved in chemical carcinogenesis, drug metabolism, and the cell cycle. In conclusion, this study developed and validated a prognostic scoring system for alcohol‑related HCC based on lncRNAs.Sterile α motif and histidine/aspartic acid domain‑containing protein 1 (SAMHD1) can inhibit reverse transcription of human immunodeficiency virus‑1 (HIV‑1) by hydrolyzing intracellular deoxy‑ribonucleoside triphosphate. However, its role in HIV‑1 disease progression has not been extensively studied. To study the impacts of SAMHD1 on HIV‑1 disease progression, especially on DNA levels, we investigated SAMHD1 levels in the peripheral blood of HIV‑1 elite controllers (ECs), antiretroviral therapy (ART) naive viremic progressors (VPs) and patients with HIV‑1 receiving ART (HIV‑ARTs) compared with healthy controls. In addition, the present study analyzed the relationship between SAMHD1 and interferon‑α, immune activation and HIV‑1 DNA levels. The results of the present study demonstrated elevated SAMHD1 expression in the peripheral blood mononuclear cells of all patients withHIV‑1, but higher SAMHD1 expression in the CD4+ T cells of only ECs compared with healthy controls. Immune activation was increased in the VPs and decreased in the ECs compared with healthy controls. Substantially lower HIV‑1 DNA levels were identified in ECs compared with those in VPs and HIV‑ARTs. SAMHD1 expression was associated with low levels of immune activation. No significant correlation was observed between SAMHD1 and HIV‑1 DNA levels. Overall, the findings of the present study indicated that SAMHD1 was highly expressed in ECs, which may be associated with low immune activation levels, but was not directly related to HIV‑1 DNA levels.Psoriasis is a common chronic inflammatory skin disease. Programmed cell death ligand 1 (PD‑L1) and programmed cell death 1 (PD‑1) are expressed on immune cells in a number of chronic inflammatory diseases. However, a limited number of studies have investigated the expression and function of the PD‑L1 and PD‑1 pathway in psoriatic inflammation. The present study used human psoriasis samples and imiquimod‑induced murine psoriasis models to investigate the potential role of PD‑1 in the modulation of psoriatic inflammation. The results demonstrated that inhibition of PD‑1 function with antibodies promoted psoriasis development. PD‑1‑fragment crystallizable (PD‑1‑Fc) treatment inhibited psoriatic inflammation and exhibited additive effects with anti‑tumor necrosis factor α therapy in imiquimod‑induced mouse psoriasis, suggesting that PD‑1‑Fc treatment may serve as a new therapeutic strategy for psoriasis.
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