Notes

Fulminant hepatic failure: A rare as well as destructive manifestation of Coronavirus condition 2019 in the 11-year-old child.
The EWS‑FLI1 fusion gene was evaluated in two patients with ES using conventional cytogenetic, fluorescence in situ hybridization and nested PCR assays, which revealed that the aberrant expression of the EWS‑FLI1 gene is accompanied by enrichment of H3K4Me3, H3K9ac and H3K27ac at the promoter region.Dysregulation of angiogenesis can be caused by hypoxia, which may result in severe diseases of the heart, including coronary artery disease. Hypoxia‑inducible factor 1 (HIF‑1) modulates angiogenesis via the regulation of several angiogenic factors. However, the underlying mechanism of hypoxia‑induced angiogenesis remains unknown. In the present study, it was hypothesized that long non‑coding RNA (lncRNA) non‑coding RNA activated by DNA damage (NORAD) may serve a role in the process of angiogenesis via the regulation of microRNA(miR)‑590‑3p under hypoxic conditions. The effect of NORAD and miR‑590‑3p on cell viability and properties associated with angiogenesis, including cell migration and tube formation in human umbilical vein endothelial cells (HUVECs) under hypoxic conditions, were assessed. Potential downstream angiogenic factors of miR‑590‑3p were also determined by molecular experiments. It was identified that NORAD expression was upregulated and miR‑590‑3p expression was downregulated in hypoxia‑expose, which highlights a potentially novel perspective for treating ischemia/hypoxia‑induced angiogenic diseases.Colorectal cancer (CRC) is one of the most common digestive tract tumors worldwide. Catalpol exerts inhibitory effects on the progression of several cancer types by regulating microRNAs (miRs). However, the precise role and carcinostatic mechanism of catalpol on CRC cells are poorly understood which limits the application of catalpol treatment. In the present study, miR‑34a and sirtuin 1 (SIRT1) expression levels were detected in CRC tissues and CRC cell lines by RT‑qPCR. Computational software analysis, luciferase assays and western blotting were used to demonstrate the downstream target of miR‑34a in CRC cells. Effects of catalpol on cell viability, apoptosis, autophagic flux and the miR‑34a/SIRT1 axis in the CRC cells were assessed by CCK‑8 assay, flow cytometry, electron microscopy and western blotting, respectively. Whether the miR‑34a/SIRT1 axis participated in catalpol‑mediated autophagy and apoptosis was investigated. The effects of catalpol on the miR‑34a/SIRT1 axis and malignant behavior were evaluated in a rat model of azoxymethane (AOM)‑induced CRC. It was revealed that miR‑34a expression levels were significantly decreased while SIRT1 was overexpressed in most of the CRC tissues and all the CRC cell lines. Clinically, a low level of miR‑34a was correlated with poor clinicopathological characteristics in CRC patients. Catalpol reduced cell viability, suppressed autophagy, promoted apoptosis, and regulated the expression of SIRT1 by inducing miR‑34a in vitro and in vivo. The autophagy‑inhibiting effect of catalpol may be a mechanism to promote apoptosis of CRC cells. miR‑34a mimic transfection resulted in autophagy‑suppressive activity similar to that of catalpol, while the miR‑34a inhibitor attenuated the antiautophagic effects of catalpol. In conclusion, miR‑34a is involved in regulating catalpol‑mediated autophagy and malignant behavior by directly inhibiting SIRT1 in CRC.Lipolysis is closely associated with obesity and insulin resistance. Berberine (BBR), a natural alkaloid derived from Coptis chinensis, has been shown to regulate lipolysis and improve insulin resistance. However, the underlying mechanism remains unclear. The present results suggested that BBR stimulated lipolysis in porcine adipocytes in a dose‑ and time‑dependent manner, which was independent of the cAMP/protein kinase A pathway. Further experimental results indicated that BBR increased phosphorylation levels of AMP‑activated protein kinase (AMPK) and adipose triglyceride lipase (ATGL), along with downregulation of Perilipin A. The AMPK inhibitor compound C significantly reversed the effect of BBR on lipolysis, Perilipin A expression and ATGL phosphorylation. Furthermore, BBR promoted expression levels of genes related to fatty acid oxidation, such as peroxisome proliferator‑activated receptor γ coactivator‑1α, mitochondrial transcription factor A, carnitine palmitoyl‑transferase‑1 and uncoupling protein 2, which were abrogated by AMPKα1 knockdown. Moreover, it was found that BBR‑induced lipolysis did not elevate serine phosphorylation of insulin receptor substrate‑1 to block insulin signaling. Collectively, the present results suggested that BBR induced lipolysis in porcine adipocytes via a pathway that involves AMPK activation, but does not cause insulin resistance.In plastic surgery, the maneuverability and safety of autologous fat transplantation have become increasingly recognized and continuously improved. However, the uncertainty of adipocyte survival makes it difficult to predict postoperative effects. Adipose‑derived stem cells (ADSCs) exhibit remarkable paracrine activity, and the number of ADSCs in adipose tissue is closely related to tissue survival. Maternally expressed gene 3 (MEG3) is known to modulate the apoptosis of various cell types. The present study aimed to evaluate the hypothesis that MEG3 serves an important role in ADSC apoptosis by regulating the expression of p53, and to explore the regulatory mechanisms of p53 in ADSC apoptosis. MEG3 was overexpressed in ADSCs and these cells were evaluated for viability, TP53 expression, apoptosis, morphology, and Bax and Bcl‑2 expression by performing MTT assays, reverse transcription‑quantitative PCR, flow cytometry analysis and western blotting. This study demonstrated that MEG3 may have an important role in the spontaneous apoptosis of ADSCs, and apoptosis induced by oxidative stress. In addition, this study revealed that p53 had a regulatory role in the downstream Bcl‑2/Bax pathway. This study provides insight into the role of MEG3 in ADSC apoptosis, thereby facilitating the survival of ADSCs during adipose tissue transplantation. Further in vivo and in vitro experiments should be conducted, along with the development of clinical applications.Hepatocellular carcinoma (HCC) has become a major cause of cancer‑related mortality worldwide. Circular RNAs (circRNAs) are non‑coding RNAs that serve important roles in multiple cancers. However, the role of circRNAs in HCC remains largely unknown. In the present study, a circRNA microarray dataset of HCC samples, GSE97332, was downloaded from the gene expression omnibus database. Following data preprocessing, differentially expressed circRNAs between HCC tissues and normal tissues were determined using GEO2R. The circRNA‑miRNA interactions were predicted by the miRanda database. The miRTarbase database was used to search for target genes of the miRNAs. A circRNA‑miRNA‑mRNA network was constructed using Cytoscape based on the obtained circRNA, miRNA and mRNA. In this network, the upregulated circRNA hsa_circRNA_100084 was found to be involved in a competing endogenous relationship of hsa_circRNA_100084‑hsa‑miR‑23a‑5p‑ insulin‑like growth factor 2 (IGF2). The differential expression of hsa_circRNA_100084, hsa‑miR‑23a‑5p and IGF2 in HCC tissues and liver cancer cells was validated by reverse transcription‑quantitative PCR. Additionally, the interactions between hsa‑miR‑23a‑5p with hsa_circRNA_100084 and IGF2 were validated by dual‑luciferase reporter assays. Knocking down hsa_circRNA_100084 inhibited the proliferation, migration and invasion of liver cancer cells, while the simultaneous overexpression of IGF2 reversed the effects of hsa_circRNA_100084 knockdown. The results show that hsa_circRNA_100084 could promote the expression of IGF2 by acting as a sponge of hsa‑miR‑23a‑5p in liver cancer cells.The present study aimed to investigate the role of matrix metalloproteinase‑1 (MMP‑1) in the development of colorectal cancer and reveal the mechanism underlying this progression. Bioinformatics methods and a public dataset were first used to analyze MMP‑1 gene expression in a public dataset. MMP‑1 expression in colorectal cancer patients was assessed by immunohistochemistry; its association with clinicopathological parameters and its significance for prognosis were analyzed. Then proliferation, scratch and Transwell assays and a xenograft model were used to assess the change in malignant behavior in cells transfected with an MMP‑1 shRNA. Changes involved in epithelial‑mesenchymal transition (EMT) and the Akt signaling pathway were detected by western blotting. According to the results, MMP‑1 expression was higher in colorectal cancer tissues than it was in matched adjacent noncancerous tissues, and its high expression was significantly related to lymphatic metastasis as well as TNM stage (P less then 0.05). Downregulation of MMP‑1 expression inhibited the progression of colorectal cancer in vitro and in vivo. Furthermore, after the cells were stably transfected with MMP‑1 shRNA, the expression of N‑cadherin, vimentin and Twist1 decreased while that of E‑cadherin increased. The expression of p‑Akt and c‑Myc also decreased. In conclusion, MMP‑1 may promote malignant behavior in colorectal cancer via EMT and the Akt signaling pathway.Osteosarcoma (OS) is the most common primary malignant tumor of the bone affecting children and adolescents. Chemotherapy is now considered as a standard component of OS treatment, not only for children, but also for adults. However, chemoresistance continues to pose a challenge to therapy. Inhibition of autophagy has been demonstrated to decrease chemoresistance in OS. Moreover, microRNA‑22 (miR‑22) inhibits autophagy, leading to an improvement in the sensitivity of cisplatin (CDDP) in OS. The aim of the present study was therefore to investigate whether miR‑22 could mediate the CDDP resistance of OS cells by inhibiting autophagy via the phosphoinositide 3‑kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway. Cell proliferation assay, LC3 flow cytometry assay and monodansylcadaverine staining in MG63 cells and CDDP resistance cells (MG63/CDDP) were performed to explore to role of miR‑22 and CDDP in OS chemoresistance. Inoculation of tumor cells in an in vivo model, reverse transcription‑quantitative effect of miR‑22. Interestingly, CDDP was demonstrated to induce autophagy by inhibiting the PI3K/Akt/mTOR pathway, whereas the pathway was upregulated in the state of chemoresistance. In conclusion, downregulation of the PI3K/Akt/mTOR pathway was shown to assist in the process of preventing chemoresistance.Inflammasomes can identify endogenous danger signals as an inflammatory immune response. As the most common inflammasome, the NLR pyrin family domain containing 3 (NLRP3) inflammasome is associated with the pathogenesis of different tumors. However, the function of the NLRP3 inflammasome in esophageal cancer (EC) has rarely been reported. Herein, the expression levels of the components of NLRP3 inflammasome and Ki‑67 were analyzed by immunohistochemistry. Furthermore, correlations between the NLRP3 inflammasome and Ki‑67 along with the clinicopathological features of EC patients were evaluated. The components of the NLRP3 inflammasome were also assessed by western blot analysis and quantitative PCR. NLRP3 was silenced or overexpressed in different esophageal squamous cell carcinoma (ESCC) cell lines, and cell viability, migration and invasion were assessed by CCK‑8 and Transwell assays. The present results showed that high NLRP3 expression in the tumor specimens was significantly associated with TNM stage and T category.
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