LncRNA Brain Cytoplasmic RNA 1 (BCYRN1) has been certified to modulate cancer cells growth and aggressiveness in several tumors. However, research about function of BCYRN1 in hepatocellular carcinoma (HCC) is limited. Therefore, our research intends to explore the function of BCYRN1 in HCC. Methods: HepG2 and BEL-7402 cell lines were employed for later function experiments. Differently expression levels of BCYRN1, miR-490-3p, and POU class 3 homeobox 2 (POU3F2) were determined on the base of TCGA dataset including 375 HCC patients and 50 normal. 370 cases of patients, which have fairly complete clinical data, were utilized for survival analysis of BCYRN1, miR-490-3p, or POU3F2 by Kaplan-Meier method. Relative expression pattern of BCYRN1 was examined by quantitative real time polymerase chain reaction (qRT-PCR), and relative expression level of POU3F2 was assessed by qRT-PCR and western blot. Cell biological behaviors were analyzed by cell counting kit-8, cloning formation, and transwell assays. Bioinformatics software and dual luciferase assay were applied to predict and confirm the targeted relationship between BCYRN1 and miR-490-3p, as well as miR-490-3p and POU3F2. Further associations among BCYRN1, miR-490-3p, and POU3F2 were analyzed by rescue assays. Results: Our results exhibited that BCYRN1 was over expressed in HCC samples, which was connected with unfavorable prognosis in HCC patients. In addition, a series of experiments exhibited that overexpression of BCYRN1 significantly expedited HCC cells growth, clone formation, and movement abilities, and vice versa. Moreover, targeted relationships between BCYRN1 and miR-490-3p, as well as miR-490-3p and POU3F2 were affirmed by dual luciferase assay. Furthermore, POU3F2 expression was negatively connected with the expression of miR-490-3p and positively associated with BCYRN1 expression. Whilst, either overexpression of miR-490-3p or knockdown of POU3F2 could remarkably inhibit the increasing trends of proliferation, clone formation, invasion, and migration abilities induced by BCYRN1 in HCC cells.

BackgroundHepatitis B virus (HBV) infection is a blood borne infectious disease that affects the liver. Human bone marrow mesenchymal stem cells (BMSCs) may serve as a cell source for adult stem cell transplantation in liver repair. However, the susceptibility of human BMSCs to HBV infection is poorly understood. The aim of this study was to investigate the infection and replication of HBV in cultures of human BMSCs.ResultsHuman BMSCs were confirmed using flow cytometry. Intracellular HBV DNA was detected at d 2 after infection and maintained at relatively high levels from d 6 to d 12. The maximal level of intracellular HBV DNA was 9.37 × 105 copies/mL. The extracellular HBV DNA was observed from d 3 to d 15, and the levels ranged from 3.792 × 102 copies/mL to 4.067 × 105 copies/mL. HBsAg in the culture medium was detected from d 2 to d 16. HBeAg secretion was positive from d 5 to d 13. HBcAg constantly showed positive signals in approximately 7%-20% of BMSCs from 2 days after exposure. Intracellular HBV covalently closed circular DNA (cccDNA) could be detected as early as 2 days postinfection, and strong signals were obtained with increasing time.ConclusionHBV can infect and replicate in human BMSCs. Human BMSCs may be a useful tool for investigating HBV life-cycle and the mechanism of initial virus-cell interactions.

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BACKGROUND Complications of vascular closure devices mainly include bleeding, vascular injury, and trapped device that cannot be removed percutaneously. However, arterial stenosis or occlusion induced by vascular injury is rare. This article introduces a rare case with severe acute limb ischemia after using the vascular closure device (StarClose). CASE SUMMARY A 54-year-old man was admitted because of necrosis of the second toe of the left foot for 2 mo. Ultrasound showed left femoral artery stenosis, and occlusion of the left popliteal, posterior tibial, peroneal, anterior tibial and dorsalis pedis arteries, suggesting arteriosclerosis obliterans of low extremities, gangrene and type 2 diabetes. He underwent an interventional procedure of drug-eluting balloon in the left lower limb via antegrade puncture of the left common femoral artery. He developed acute limb ischemia after 1 h, and severe pain, numbness, pale skin, low skin temperature and weakened sensation in the left foot. Injury of the common femoral artery intima was considered. Exploratory surgery showed occlusion at the puncture point accompanied with bulged vascular lumen and flipped vascular intima caused by StarClose. The flipped intima was removed. The limb blood supply was restored and the limb was saved post-surgery. He recovered well at final follow-up. CONCLUSION Incorrect use of the vascular closure device was the main cause of severe acute limb ischemia in this case.

Background Diabetic foot ulcer (DFU) is one of the most serious complications of diabetes and the main cause of non-traumatic amputation in diabetic patients. Disruption of alternative splicing (AS) and RNA binding proteins (RBPs) has been proven to cause a variety of diseases, including DFU. But the regulatory network of RBPs-AS and its underlying functions in DFU remain unclear. Methods Whole transcriptome data of ulceration tissues were analyzed to identify dysregulated AS and RBPs, comprising ulceration tissues from thirteen DFU patients (seven patients with healed ulcers and six patients with unhealed ulcers, the DFU group) and eight normal samples (the control group). We identified the differentially expressed genes (DEGs), regulated alternative splicing events (RASEs), and changes in immune infiltration between DFU and control tissues. Finally, co-expression analysis was performed to establish the regulatory network of RBPs-AS-immune infiltration in DFU tissues. Results DEG analysis showed that 4478 and 4514 genes were differentially expressed in healed and unhealed DFU tissues, respectively. Gene functional analysis showed that many DEGs were enriched in immune and inflammatory pathways. Many RASEs were identified between unhealed DFU and control tissues. Functional analysis showed that genes with RASEs were primarily enriched in apoptosis pathways. According to immune infiltration analysis, the percentage of memory B cells and activated mast cells were higher in the DFU group than in the control group. According to the co-expression analysis, the ratio values of RASEs in apoptosis-associated genes were related to the percentage of infiltrated immune cells in DFU tissues. In addition, the co-expression network showed that differentially expressed RBPs (DE RBPs) could regulate the RASEs and affect the immune infiltration in DFU tissues. Finally, we found that the aberrant expressions of DCN, HSP90AA1, SMAD7, YWHAG, YWHAZ, KPNA2, S100A16, and DUSP14 would affect the AS of FAT1, COL12A1, UPP1, EIF5A and AKAP13 in DFU tissues. Conclusion Our results showed that DE RBPs may play a role in wound healing in DFU by regulating the AS of pre-mRNAs, especially immune inflammation- and apoptosis-related pre-mRNAs, and may continue to play a role in DFU regardless of the healing state.