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Lung adenocarcinoma (LUAD) is the most predominant subtype of non-small cell lung cancer (NSCLC) that is experiencing the fastest growth rate in incidence. Chemoresistance and the presence of cancer stem cells are considered to be the main obstacles preventing the successful treatment of patients with NSCLC, the molecular mechanism of which remains poorly understood. The present study aimed to investigate the effects of microRNA (miR)-140-3p on cisplatin sensitivity and stem cell-like properties of LUAD cells. Analysis of publicly available data demonstrated that miR-140-3p expression was downregulated in LUAD, and positively associated with the overall survival rate of patients. In addition, transfection with the miR-140-3p mimic reduced LUAD cell viability and induced apoptosis following treatment with cisplatin whilst decreasing stem cell-like properties. miR-140-3p overexpression was also found to attenuate cisplatin resistance and reduce stem cell-like properties in LUAD cells by suppressing Wnt/β-catenin signaling, all of which were reversed by the overexpression of β-catenin. Taken together, results of the present study suggest miR-140-3p to be an effective therapeutic strategy for patients with LUAD.Osteoarthritis (OA) is a joint disease caused by a variety of factors, including aging, obesity and trauma. MicroRNAs (miRNAs) have been reported to be crucial regulators during OA progression. The present study aimed to investigate the role of miR-17-5p and miR-19b-3p during OA development. Interleukin (IL)-1β-treated chondrocytes were used to mimic OA in vitro. The expression levels of miR-17-5p and enhancer of zeste homolog 2 (EZH2) were measured in cartilage tissues and chondrocytes using reverse transcription-quantitative PCR or western blotting. Apoptosis was assessed by flow cytometry. The protein expression levels of extracellular matrix (ECM)-associated genes were detected by western blotting. The binding sites between miR-17-5p or miR-19b-3p and EZH2 were predicted using the MicroT-CDS online database and verified using dual-luciferase reporter and RIP assays. miR-17-5p expression was downregulated, whereas EZH2 expression was upregulated in OA cartilage tissues and IL-1β-induced chondrocytes compared with that in the control tissues and cells. miR-17-5p mimics inhibited IL-1β-induced apoptosis and ECM degradation in chondrocytes. EZH2 was the target of miR-17-5p and miR-19b-3p in chondrocytes, and enhanced apoptosis and ECM degradation in IL-1β-stimulated chondrocytes. Rescue experiments revealed that miR-17-5p or miR-19b-3p mimic-induced inhibition of OA progression was reversed by EZH2 overexpression. In conclusion, miR-17-5p and miR-19b-3p inhibited OA progression by targeting EZH2, which may serve as a potential therapeutic target for OA.Non-small cell lung cancer (NSCLC) is a type of cancer that is associated with high prevalence and high mortality rates in China. Therefore, it is of importance to identify the mechanisms underlying NSCLC progression. In the present study, reverse transcription-quantitative PCR was performed to measure the expression of microRNA (miR)-365b in NSCLC cell lines. In addition, the biological roles of miR-365b and N-acetylgalactosaminyltransferase 4 (GALNT4) were investigated by manipulating the expression levels of miR-365b and GALNT4 in NSCLC cells. It was found that miR-365b expression was reduced in NSCLC tissues and cells. Overexpression of miR-365b inhibited NSCLC cell proliferation whilst promoting apoptosis, but miR-365b knockdown promoted NSCLC cell proliferation. In addition, it was demonstrated that miR-365b regulated the proliferation and apoptosis of NSCLC cells by targeting GALNT4 expression. Collectively, the present study identified a miR-365b/GALNT4 regulatory axis in NSCLC, suggesting that miR-365b may serve as a therapeutic target for NSCLC.Potential use of sonographic TI-RADS classification combined with circulating miRNA expression profiling in the diagnosis of thyroid nodules was explored. Retrospective analysis was performed on clinical data of 121 patients with thyroid nodules. The biopsy specimens of patients obtained through ultrasound-guided aspiration and blood specimens were evaluated in Zhengzhou Central Hospital Affiliated to Zhengzhou University from June 2018 to June 2019. In addition, the blood specimen test results of 121 healthy volunteers (control group) who underwent physical examination were retrospectively analyzed. Results of sonographic TI-RADS classification and circulating miRNA expression profiling were compared with the pathological results. Of the 212 nodules, 2 fell into TI-RADS category 2 and were diagnosed as benign. Malignant nodules accounted for 4.35, 37.14, 84.78, 93.33 and 96.77% of those nodules that fell into TI-RADS categories 3, 4a, 4b, 4c and 5, respectively. Of the 121 patients, 92.55% had with nodular goiter, 3.31% had inflammatory nodules, 2.48% toxic nodular goiter, 0.83% thyroid cysts and 0.83% thyroid tumors. A nodule that fell into a higher TI-RADS classification category had a higher risk of malignancy. The expression levels of miRNA146b, miRNA187, miRNA375, miRNA-222-3p and miRNA-151a-5p were higher, while the level of miRNA138 was lower, in patients with either benign or malignant thyroid nodules compaed to those in the control group. The expression levels of miRNA146b, miRNA187, miRNA375, miRNA-222-3p and miRNA-151a-5p were higher, while the level of miRNA138 was lower, in patients with malignant thyroid nodules than those in patients with benign thyroid nodule (P less then 0.05). The AUC of the combined diagnostic method was 0.973, which was significantly different from the AUCs of the individual diagnostic method (P less then 0.05). In conclusion, sonographic TI-RADS classification combined with circulating miRNA expression profiling can improve the diagnosis of thyroid nodules.In the present study, the association between the severity of coronary artery disease (CAD) and myeloperoxidase (MPO), homocysteine (Hcy) and high-sensitivity C-reactive protein (hs-CRP) was assessed and their diagnostic and prognostic value was determined. A total of 112 patients with CAD [patient group (PG)] and 112 healthy participants who visited the hospital for physical examinations [control group (CG)] were enrolled in the present study. The plasma levels of MPO, Hcy and hs-CRP were compared between the two groups. According to the arteriography results, the patients were further divided into the single-vessel disease group (SVG), double-vessel disease group (DVG) and multi-vessel disease group (MVG). The Gensini scores of the three groups were evaluated according to the Gensini score standard. The correlations between the expression of MPO, Hcy or hs-CRP and the Gensini score of the PG were analyzed. The patients' major adverse cardiovascular event (MACEs) were recorded over 6 months and compared, andless then 0.05). The area under the curve (AUC) and sensitivity for MPO levels to predict MACEs were higher than those of Hcy and hs-CRP (P less then 0.05); however, there was no significant difference in the AUC and sensitivity of Hcy and hs-CRP for predicting MACEs (P less then 0.05). The specificity of hs-CRP for predicting MACEs was higher than that of MPO and Hcy (P less then 0.05). click here The number of lesions, hypertension, diabetes, MPO, Hys and hs-CRP were determined to be independent risk factors for MACEs. In conclusion, for patients with CAD, elevated plasma levels of MPO, Hcy and hs-CRP were directly correlated with the severity of CAD and the risk of MACEs. Furthermore, MPO, Hcy and hs-CRP may effectively predict MACEs and are of important clinical significance in terms of judging the condition and improving the prognosis for patients with CAD.Expression levels of miR-223-3p and NLRP3 in high glucose and high fat (HGHF)-induced diabetic mice, and the mechanism on the injury of mouse cardiac microvascular endothelial cells (MCMECs) were investigated. Four-week C57BL/6J laboratory mice were selected and randomized into a control group and a model group (n=10 each). Mice in the model group were fed with HGHF diet to establish a mouse model of diabetes. Further MCMECs were purchased to construct carriers through transient transfection, and were separated into a normal group (cultured in the normal environment), a model group (not transfected), a blank carrier group (transfected with miR-NC), a miR-223-3p-mimics group, and a miR-223-3p-inhibitor group. RT-qPCR was used to detect the expression levels of miR-223-3p and NLRP3, and western blot analysis to detect the expression levels of NLRP3, apoptosis-related proteins Bax and caspase-3, and anti-apoptotic protein Bcl-2. Flow cytometry was used to observe apoptosis and TargetScan to predict the target relationship between miR-223-3p and NLRP3. Dual-luciferase reporter gene assay was used to detect the relationship between miR-223-3p and NLRP3. Compared with those in the control group, the mice in the model group had significantly lower expression of miR-223-3p. However, significantly higher mRNA and protein expression levels of NLRP3 were observed (P less then 0.05). After modeling, miR-223-3p overexpression downregulated the expression levels of NLRP3 mRNA, Bax and NLRP3 protein, as well as inhibited endothelial cell apoptosis (P less then 0.05), while the inhibition of miR-223-3p expression upregulated the expression levels and promoted apoptosis. In conclusion, miR-223-3p expression is low, however, NLRP3 is highly expressed in the heart tissue of HGHF-induced diabetic mice. miR-223-3p reduces the injury of MCMECs and inhibits endothelial cell apoptosis in mice by regulating the expression of NLRP3.Correlation between fecal calprotectin (FC) and endoscopic activity assessed by Ulcerative Colitis Endoscopic Index of Severity (UCEIS) in acute severe colitis (ASC) patients was explored to evaluate the predictive value of FC in clinical outcomes. Seventy-one ASC patients were retrospectively evaluated. FC level within 3 days of colonoscopy was measured with ELISA. Demographic and clinical data, laboratory parameters, and medical therapy were documented, and the endoscopic severity of disease was rated by UCEIS. The end points were the rate of failed corticosteroid therapy, colectomy, and mortality. There was significant correlation between UCEIS and FC level (r=0.729, P1672 µg/g, sensitivity and specificity were 80.2 and 66.7%, respectively, in prediction for colectomy using receiver operating characteristics analysis. The results indicated that FC, as a non-invasive indicator, correlates positively with the UCEIS. Baseline FC level predicts clinical outcomes in ASC patients, which make a timely treatment strategy conversion possible after accurately forecasting the likelihood of failure of intravenous steroid therapy.A number of previous studies have demonstrated that inhibiting autophagy can increase the cellular cytotoxicity of chemotherapeutic agents in urothelial cancer cells. However, the mechanistic roles of autophagy in gemcitabine (GEM) resistant bladder cancer cells have not been thoroughly investigated. In the present study, immunohistochemistry staining of autophagy marker LC3 was performed in bladder cancer and healthy control tissues and demonstrated an essential role of autophagy in cancer development. A GEM-resistant cell line was established to assess the effects of autophagy on the acquisition of GEM resistance. Western blotting of autophagy markers in GEM-resistant bladder cancer cells suggested that GEM resistance was caused, at least partially, by GEM-induced autophagy. GEM resistance was demonstrated to be reversed by the inhibition of autophagy by 3-methyladenine. In addition, oblongifolin C (OC), a novel autophagic flux inhibitor purified from traditional Chinese medicine, was found to enhance the efficiency of GEM in GEM-resistant bladder cancer cells by inhibiting autophagic flux.