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MicroRNAs (miRs) serve an important role in cell differentiation, proliferation and apoptosis by negatively regulating gene expression at the transcriptional or post‑transcriptional level. EI24 autophagy associated transmembrane protein (EI24) is a tumor suppressor gene that serves an important role in the occurrence and development of digestive system tumors. However, little is known regarding the relationship between EI24 and the prognosis of patients with colorectal cancer (CRC). Our previous study confirmed EI24 as the target molecule of miR‑483, using reporter gene detection. Thus, the aim of the present study was to elucidate the effect of the abnormal expression of miR‑483 on the malignant phenotype of CRC through a series of cell function experiments and nude mice tumorigenicity experiments, and to determine the expression level of EI24, a downstream target gene of miR‑483, in CRC and its relationship with patient prognosis. In CRC tissues and cells, the expression level of miR‑483 was upregulated, while the expression level of EI24 was downregulated. Cell function tests such as MTT assay, cell cycle assay, colony formation assay, Migration and invasion assays and nude mice tumorigenicity experiments demonstrated that the overexpression of miR‑483 promoted the proliferation, invasion and metastasis of CRC. Moreover, the reverse transcription‑quantitative PCR results indicated that overexpression of miR‑483 inhibited the expression level of EI24. The relationship between the clinical data and immunohistochemical results from 183 patients with CRC and survival was examined. It was found that the expression level of EI24 was positively associated with the prognosis of patients. As a cancer‑promoting factor, miR‑483 enhances the proliferation, migration and invasion of CRC cells by reducing the expression level of EI24.Cigarette smoking is the leading cause of all histological types of lung cancer, and the role that microRNAs (miRNAs) serve in its pathogenesis is being increasingly recognized. The aim of the present study was to investigate the role of miR‑200b on migration in cigarette smoke‑induced malignant transformed cells. In the present study, miR‑200b expression was found to be increased in cigarette smoke (CS)‑exposed BEAS‑2B cells, lung cancer cell lines and tumor tissue samples. Using wound healing and Transwell migration assays, the migratory ability was shown to be increased in miR‑200b‑overexpressing cells, whereas miR‑200b knockdown resulted in reduced migration. Additionally, the expression of E‑Cadherin was downregulated, whereas that of N‑Cadherin was upregulated in miR‑200b mimic‑transfected cells, suggesting an increase in epithelial‑mesenchymal transition. Downstream, using four target gene prediction tools, six target genes of miR‑200b were predicted, amongst which, ETS proto‑oncogene 1 transcription factor (ETS1) was shown to be significantly associated with tumor invasion depth and negatively associated with miR‑200b expression. The interaction between miR‑200b and ETS1 was confirmed using a dual‑luciferase reporter assay. Using rescue experiments, the increased migratory ability of the miR‑200b‑overexpressing cells was reversed by ETS1 overexpression. In summary, this study showed that miR‑200b overexpression serves a carcinogenic role and promotes the migration of BEAS‑2B cells following long‑term exposure to CS by targeting ETS1.Aberrant expression of microRNAs (miRNAs/miRs) is associated with the initiation and progression of colorectal cancer (CRC), but how they regulate colorectal tumorigenesis is still unknown. The present study was designed to investigate the expression profile of miRNAs in human CRC tissues, and to reveal the molecular mechanism of miRNA‑142‑3p in suppressing colon cancer cell proliferation. The expression of miRNA was examined using an Exiqon miRNA array. Bioinformatics was used to predict the target genes of differentially expressed miRNAs and to analyze their biological function in CRC. The effect of miR‑142‑3p in colon cancer cells was evaluated in vitro using cell proliferation, colony formation and Transwell assays. Dual‑luciferase reporter gene assays were performed to investigate the association between miR‑142‑3p and Rac family small GTPase 1 (RAC1). The effect of miR‑142‑3p regulation on colon cancer proliferation was assessed through western blotting and quantitative polymerase chain reaction analysing.GATA binding protein 1 (GATA‑1) is one of the most important hematopoietic transcription factors in the production of blood cells, such as platelets, eosinophils, mast cells and erythrocytes. GATA‑1 regulates the participation of microRNA (miRNAs/miRs) in erythroid differentiation under normoxia. However, GATA‑1 expression and the regulation of miR‑210‑3p in the context of erythroid differentiation under hypoxia remain unknown. The present study examined the expression levels of GATA‑1 and miR‑210‑3p in the model of erythroid differentiation in K562 cells under hypoxia, and determined the effects of GATA‑1, miR‑210‑3p and SMAD2 on erythroid differentiation through lentivirus transfection experiments. The present study detected increased GATA‑1 expression under hypoxia. Moreover, miR‑210‑3p was identified as a positive regulator of erythroid differentiation, which was upregulated both during erythroid differentiation and in GATA‑1 overexpression experiments under hypoxia. Importantly, in the K562 cell model of erythroid differentiation under hypoxia, miR‑210‑3p was upregulated in a GATA‑1‑dependent manner. Using a double luciferase reporter assay, miR‑210‑3p was identified as a downstream target of GATA‑1‑mediated regulation of erythropoiesis. Gain‑ or loss‑of‑function analysis of miR‑210‑3p identified its importance in erythroid differentiation. Furthermore, it was found that SMAD2 may be a downstream target gene for miR‑210‑3p. Bioinformatics predictions suggested that SMAD2 mediated miR‑210‑3p‑induced regulation of erythroid differentiation. Collectively, the present study provides novel insights into the miRNA regulation of erythroid differentiation.Recent studies have reported that methylmercury (MeHg) induces neuronal apoptosis, which is accompanied by abnormal neurological development. Despite the important role of docosahexaenoic acid (DHA) in maintaining the structure and function of the brain, as well as improving neuronal apoptosis induced by MeHg, the exact mechanism remains unknown. The present study hypothesized that the reactive oxygen species (ROS)‑mediated JNK signaling pathway may be associated with the protective effect of DHA against MeHg‑induced PC12 cell apoptosis. Cell Counting Kit‑8, TUNEL staining, flow cytometry, ROS detection, PCR and western blot analysis were performed. The results demonstrated that MeHg inhibited the activity of PC12 cells, causing oxidative damage and promoting apoptosis; however, DHA significantly attenuated this effect. Mechanistic studies revealed that MeHg increased intracellular ROS levels and JNK protein phosphorylation, and decreased the expression levels of the anti‑apoptotic protein Bcl‑2, whereas DHA reduced ROS levels and JNK phosphorylation, and increased Bcl‑2 expression. In addition, the ROS inhibitor N‑acetyl‑l‑cysteine (NAC) was used to verify the experimental results. After pretreatment with NAC, expression levels of Bcl‑2, Bax, phosphorylated‑JNK and JNK were assessed. Bcl‑2 protein expression was increased and the Bcl‑2/Bax ratio was increased. Moreover, the high expression levels of phosphorylated‑JNK induced by MeHg were significantly decreased. Based on the aforementioned results, the present study indicated that the effects of DHA against MeHg‑induced PC12 cell apoptosis may be mediated via the ROS/JNK signaling pathway.Soluble fibrinogen‑like protein 2 (sFGL2), as a novel effector of regulatory T cells (Tregs), exhibits immune regulatory activity in several inflammatory diseases. Immune activation and persistent inflammation participate in the progression of ischemic heart failure (IHF). The present study aimed to determine serum sFGL2 levels in patients with IHF and explore the relationship between sFGL2 levels and cardiac function. A total of 104 patients with IHF and 32 healthy controls were enrolled. patients with IHF were further split into subgroups according to the New York Heart Association functional classification or left ventricular ejection fraction (LVEF). Serum sFGL2 levels and peripheral Tregs frequencies were analyzed by ELISA and flow cytometry, respectively. The suppressive function of Tregs was measured by proliferation and functional suppression assays. Serum levels of sFGL2 and circulating Tregs frequencies were significantly decreased in patients with IHF compared with healthy controls. In patients with IHF, sFGL2 levels and Tregs frequencies were decreased with the deterioration of cardiac function. Tregs from patients with IHF exhibited compromised ability to suppress CD4+CD25‑ T cells proliferation and inflammatory cytokines secretion. PCNA-I1 manufacturer Specifically, sFGL2 levels and Tregs frequencies positively correlated with LVEF, whereas negatively correlated with left ventricular end‑diastolic dimension and N‑terminal pro‑brain natriuretic peptide. sFGL2 levels were positively correlated with Tregs frequencies. In conclusion, the reduction of serum sFGL2 levels are associated with the progression of IHF and sFGL2 could be used as a potential indicator for predicting disease severity.As is well known, dexmedetomidine (DEX) serves a neuroprotective role in cerebral ischemia‑reperfusion (CIR) injury, and microRNA (miR)‑199a has been re‑ported to be associated with IR injury. However, the association between DEX and miR‑199a in CIR injury remains unknown. Thus, the aim of the present study was to verify whether the neuroprotective effect of DEX on cerebral ischemia‑reperfusion rats is associated with miR‑199a. A rat model of CIR was established, and the modified neurological severity score (mNSS) was evaluated. The effect of DEX on the patholog‑ical structure of the cerebral cortex in CIR rats was observed by hematoxylin and eosin and Nissl staining. Reverse transcription‑quantitative PCR was used to analyze the expression levels of miR‑199a in brain tissue following intracerebroventricular injection of miR‑199a antagomir. The co‑expression of NeuN and microtubule‑associated proteins 1A/1B light chain 3B in the cerebral cortex was analyzed by immunofluorescence staining. Western blotting and immunohistochemistry were performed to analyze the expression of autophagy‑associated proteins in the brain tissue. DEX inhibited the expression of miR‑199a, decreased the mNSS and improved pathological damage to the cerebral cortex. DEX also inhibited autophagy and expression levels of associated proteins and decreased nerve cell injury. In conclusion, DEX inhibited expression of miR‑199a and improved neurocyte injury induced by CIR.Cancer metastasis and recurrence are major causes of poor survival in patients with colorectal cancer (CRC). Therefore, the biological behavior of microRNA (miR)‑451 in CRC deserves further investigation. Reverse transcription‑quantitative PCR was applied to measure the relative expression of miR‑451 in blood serum specimens from patients with CRC and CRC cells. In vitro, HCT116 cells were transfected with miR‑451 mimics, a miR‑451 inhibitor, or SAMD4B plasmids. Proliferation, migration and apoptosis were measured using CCK‑8, Transwell assays and flow cytometry, respectively. Luciferase reporter assay was used to identify targets of miR‑451 and western blotting performed to explore the internal mechanisms of miR‑451 regulation. In vivo, the effect of miR‑451 and SAMD4B plasmids on tumor growth was analyzed using a nude mouse xenograft model. Results indicated that serum miR‑451 expression was lower in patients with CRC compared with healthy controls. Patients with elevated expression of miR‑451 had longer survival times compared with those with low expression.