Notes

Ovarian Cancer-Associated Ascites Have Substantial Proportions associated with Cytokine-Responsive CD56bright NK Tissues.
Fibroblast growth factor 23 (FGF23) is a bone-derived hormone that regulates renal phosphate reabsorption and vitamin D synthesis in renal proximal tubules. High circulating FGF23 levels are associated with increased mortality in patients with chronic kidney disease and those on dialysis. Current data also suggest higher circulating levels of FGF23 are associated with cardiovascular mortality, vascular calcification, and left ventricular hypertrophy; however, evidence on the role of FGF23 in patients on dialysis is incomplete, and some of the data, especially those on cardiovascular disease (CVD), are controversial. This study aimed to evaluate factors associated with FGF23 in hemodialysis patients with or without CVD. Randomly selected 76 patients on maintenance hemodialysis at a single hemodialysis center were enrolled. After the exclusion of eight patients with extremely outlying FGF23 levels, 68 patients, including 48 males and 46 patients with a CVD history, were included in the study. learn more The mean age was 6ted with lower FGF23 levels in patients with CVD.Galectin‑3 is expressed in various tissues and plays an important role in the tumor microenvironment (TME). Galectin‑3 has been found to be overexpressed in a variety of cancers and is associated with tumor progression and metastasis. Over the past decades, emerging evidence has suggested that the TME may induce galectin‑3 expression to maintain cellular homeostasis and promote cell survival. Furthermore, galectin‑3 regulates immune cell function to promote tumor‑driven immunosuppression through several mechanisms. In the TME, intracellular and extracellular galectin‑3 has different functions. In addition, it has been reported that galectin‑3 is associated with glycolysis and mitochondrial metabolism in tumors, and it is involved in the regulation of relevant signaling pathways, thus promoting cancer cell survival via adapting to the TME. The aim of the present review was to summarize the current knowledge on galectin‑3 production and its function in the TME, its effect on TME immunosuppression, its association with tumor metabolism and relevant signaling pathways, and to report common types of cancer in which galectin‑3 is highly expressed, in order to ensure a comprehensive understanding of the critical effects of galectin‑3 on tumor progression and metastasis.Double‑stranded RNA‑binding protein Staufen homolog 1 (STAU1) is a highly conserved multifunctional double‑stranded RNA‑binding protein, and is a key factor in neuronal differentiation. RNA sequencing was used to analyze the overall transcriptional levels of the upregulated cells by STAU1 and control cells, and select alternative splicing (AS). It was determined that the high expression of STAU1 led to changes in the expression levels of a variety of inflammatory and immune response genes, including IFIT2, IFIT3, OASL, and CCL2. Furthermore, STAU1 was revealed to exert a significant regulatory effect on the AS of genes related to the 'nerve growth factor receptor signaling pathway'. This is of significant importance for neuronal survival, differentiation, growth, post‑damage repair, and regeneration. In conclusion, overexpression of STAU1 was associated with immune response and regulated AS of pathways related to neuronal growth and repair. In the present study, the whole transcriptome of STAU1 expression was first analyzed, which laid a foundation for further understanding the key functions of STAU1.E2F transcription factor 5 (E2F5) is a member of the E2F family of transcription factors, which are involved in regulation of various cellular processes, including cellular proliferation, apoptosis, differentiation and DNA damage response. Previously, we reported that E2F5 was aberrantly overexpressed in estrogen receptor (ER)‑negative breast cancer, especially in triple‑negative breast cancer (TNBC). In the present study, it was revealed that E2F5 gene silencing caused a significant reduction in the proliferation rate of breast cancer MCF7 (ER‑positive luminal‑type) and MDA‑MB‑231 (TNBC‑type) cells. Additional experiments demonstrated that E2F5 knockdown triggered cell death of MCF7 cells but not MDA‑MB‑231 cells. As MCF7 and MDA‑MB‑231 cells carry wild‑type and mutant TP53, respectively, and BT474 (ER‑negative, HER2‑positive type) carrying mutant TP53 exhibited similar results to MDA‑MB‑231, the possible effects of E2F5 gene depletion on cell death‑related TP53‑target gene expression were examined. Real‑time RT‑qPCR analysis revealed that knockdown of E2F5 in MCF7 cells stimulated cell death‑related transcription of TP53‑target genes such as BAX, NOXA and PUMA. For MDA‑MB‑231 and BT474 cells, E2F5 gene silencing revealed marginal effects on the expression of TP53 target genes. In addition, silencing of TP53 abrogated the effect of E2F5 silencing in MCF7 cells. Collectively, the present results indicated that E2F5 participated in the carcinogenesis of breast cancer carrying wild‑type TP53 through suppression of TP53, while E2F5 had a pro‑proliferative but not anti‑apoptotic effect on breast cancer with TP53 mutation.Tetralogy of Fallot (TOF) is the most common form of cyanotic congenital heart disease (CHD). Although a lower methylation level of whole genome has been demonstrated in TOF patients, little is known regarding the DNA methylation changes in specific gene and its associations with TOF development. NOTCH4 is a mediator of the Notch signalling pathway that plays an important role in normal cardiac development. However, the role of epigenetic regulation of the NOTCH4 gene in the pathogenesis of TOF remains unclear. Considering the NOTCH4 low mutation frequency and reduced expression in the TOF patients, we hypothesized that abnormal DNA methylation change of NOTCH4 gene may influence its expression and responsible for TOF development. In this study, we measured the promoter methylation status of NOTCH4 and was measured and its regulation mechanism was explored, which may be related to TOF disease. Additionally, the promoter methylation statuses of NOTCH4 was measured in order to further understand epigenetic mechtion at the putative ETS1 binding sites. These findings suggested that decreased NOTCH4 expression in patients with TOF may be associated with hypermethylation of CpG site 2 in the NOTCH4 promoter region, due to impaired binding of ETS1.Ras‑GTPase‑activating protein SH3 domain‑binding protein 1 (G3BP1) has been reported to be of importance in the occurrence and development of colon cancer. However, the underlying mechanisms remain largely unknown. Therefore, the aim of the present study was to investigate the role of Wnt/β‑catenin signaling in G3BP1‑mediated colon cancer progression. The expression of G3BP1 in colon tissues and cells was detected via reverse transcription‑quantitative PCR, western blotting and immunohistochemistry. Gain‑of‑function assays were performed in colon cancer RKO cells, which have a relatively low expression of G3BP1, while loss‑of‑function assays were performed in SW620 colon cancer cells, which have a relatively high expression of G3BP1. Cell proliferation, apoptosis and tumorigenesis were assessed using Cell Counting Kit‑8, flow cytometry and tumor‑bearing mice assays, respectively. The results demonstrated that G3BP1 expression was significantly upregulated in colon cancer tissues and cells compared with healthy colon tissues and cells. It was found that high expression of G3BP1 was closely associated with the poor prognosis and advanced clinical process in patients with colon cancer. Overexpression of G3BP1 in RKO cells enhanced their proliferative ability and decreased their apoptosis tendency, while knockdown of G3BP1 inhibited SW620 cell proliferation and induced apoptosis. In addition, G3BP1 interacted with β‑catenin and upregulated its expression and nuclear accumulation. It was identified that β‑catenin knockdown abolished the effects of G3BP1 on the enhancement of cell proliferation in vitro and tumor formation in vivo, as well as the inhibition of cell apoptosis. In conclusion, the present study demonstrated that G3BP1 promoted the progression of colon cancer by activating β‑catenin signaling, which provided novel evidence for the role of G3BP1 in colon cancer.Gastric cancer (GC) is one of the most common types of malignant tumor and it demonstrates high mortality rates. The majority of cases of GC are diagnosed at an advanced stage, which seriously endangers the health of the patient. Therefore, discovering a novel diagnostic method for GC is a current priority. Exosomes are 40 to 150‑nm‑diameter vesicles consisting of a lipid bilayer secreted by a variety of cells that exist in multiple different types of body fluids. Exosomes contain diverse types of active substances, including RNAs, proteins and lipids, and play important roles in tumor cell communication, metastasis and neovascularization, as well as tumor growth. Non‑coding RNAs (ncRNAs) do not code proteins, and instead have roles in a variety of genetic mechanisms, such as regulating the structure, expression and stability of RNAs, and modulating the translation and function of proteins. In recent years, exosomal ncRNAs have become a novel focus in research. An increasing number of studies have demonstrated that exosomal ncRNAs can be used in the prediction and treatment of GC. The present review briefly discusses the role of exosomal ncRNAs as a potential biomarker, and summarizes important regulatory genes involved in the development and progression of GC.Acute lymphoblastic leukaemia (ALL) is a malignant proliferative disease that originates from B‑lineage or T‑lineage lymphoid progenitor cells. Resistance to chemotherapy remains an important factor for treatment failure. The aim of the present study was to investigate drug resistance in T‑cell ALL (T‑ALL). Bioinformatics analysis of Oncomine and Gene Expression Omnibus data was performed to evaluate the expression of haematopoietic SH2 domain containing (HSH2D) in various lymphomas. HuT‑78 cells with HSH2D overexpression and or knockdown were constructed, and the effect on related downstream signalling molecules was detected. To study the effect of HSH2D on methotrexate (MTX) resistance, cell cycle and apoptosis analyses were conducted using flow cytometry, and MTT and EdU assays were used to detect the effect of MTX resistance and HSH2D gene expression on the biological function of HuT‑78 cells. Via the analysis of the data sets, it was identified that the expression of HSH2D was downregulated in T‑ALL compared with B‑cell ALL. Western blotting and reverse transcription‑quantitative PCR demonstrated that the overexpression of HSH2 resulted in the inhibition of CD28‑mediated IL‑2 activation. In related experiments with drug‑resistant cell lines, it was determined that HSH2D expression is necessary for HuT‑78 cells to be resistant to MTX. In conclusion, the results suggested that HSH2D serves an important role in the resistance of T‑ALL to MTX, which provides a potential research target for the study of drug resistance of T‑ALL.
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