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Previous studies have identified microRNA (miRNA/miR)‑3613‑3p as a heat stress (HS)‑related miRNA in endothelial cells that can lead to apoptosis. However, the mechanism underlying the miR‑3613‑3p‑mediated apoptosis of HS‑exposed endothelial cells remains unclear. In the present study, western blot analysis and reverse transcription‑quantitative PCR were used to determine protein and miRNA expression levels, respectively. Annexin V‑fluorescein isothiocyanate/propidium iodide staining, caspase‑3 activity measurements and DNA fragmentation assays were performed to detect apoptosis. To evaluate whether mitogen‑activated protein kinase kinase kinase 2 (MAP3K2) was a direct target of miR‑3613‑3p, a luciferase reporter assay was performed. In addition, transient transfection was used to carry out loss‑ and gain‑of‑function experiments. The results revealed that miR‑3613‑3p expression was reduced in human umbilical vein endothelial cells (HUVECs) following HS, which led to apoptosis. Mechanistically, following HS, a decrease in miR‑3613‑3p binding to the 3'‑untranslated region of MAP3K2 directly upregulated its expression, and the downstream p38 and caspase‑3 pathways, thereby leading to apoptosis. Taken together, the results of the present study demonstrated that HS suppressed miR‑3613‑3p expression, which activated the MAP3K2/p38/caspase‑3 pathway, leading to the apoptosis of HUVECs. In conclusion, the miR‑3613‑3p/MAP3K2/p38/caspase‑3 pathway may serve an indispensable role in regulating the progression of apoptosis, indicating a regulatory role of miR‑3613‑3p in the pathophysiology of HS‑exposed endothelial cells.Neutrophilic asthma (NA) is a subtype of asthma that responds poorly to corticosteroid treatment. In certain diseases, microRNA (miR)‑29a‑3p is considered to be a key regulatory molecule for remodeling of the extracellular matrix. However, the effect of miR‑29a‑3p on airway remodeling is unknown. The present study aimed to investigate the role of miR‑29a‑3p in NA. A mouse model of NA was established and these animals were compared to normal controls. Both groups of mice were subjected to lung function tests and histopathological analysis. Human bronchial epithelial cells (16HBE) were grown in culture and incubated with secreted protein acidic rich in cysteine (SPARC) and a miR‑29a‑3p mimic. The expression of miR‑29a‑3p, SPARC and epithelial‑mesenchymal transition (EMT)‑related markers were measured using reverse transcription‑quantitative PCR and western blotting. Luciferase reporter assay was performed to identify the direct regulatory relationship between miR‑29a‑3p and SPARC. miR‑29a‑3p expression was significantly decreased, while SPARC expression was increased in the NA mouse model with a phenotype of EMT. Overexpression of SPARC downregulated the expression of E‑cadherin, while it increased the expression of vimentin in 16HBE cells. miR‑29a‑3p administration reversed the SPARC‑induced effects on E‑cadherin and vimentin expression. Luciferase assays confirmed that SPARC was the target gene for miR‑29a‑3p. Furthermore, SPARC overexpression increased the protein expression of phosphorylated (p)‑ERK, while transfection with miR‑29a‑3p mimics significantly inhibited this increase. The data suggested that EMT in the NA mouse model was associated with decreased levels of miR‑29a‑3p and elevated SPARC. Furthermore, SPARC could induce the formation of EMT in 16HBE cells in vitro and this was directly targeted by miR‑29a‑3p and mediated by p‑ERK, suggesting that miR‑29a‑3p may participate in the airway remodeling of NA.Tissues have remarkable natural capabilities to regenerate for the purpose of physiological turnover and repair of damage. Adult mesenchymal stem cells (MSCs) are well known for their unique self‑renewal ability, pluripotency, homing potential, paracrine effects and immunomodulation. Advanced research of the unique properties of MSCs have opened up new horizons for tissue regenerative therapies. However, certain drawbacks of the application of MSCs, such as the low survival rate of transplanted MSCs, unsatisfactory efficiency and even failure to regenerate under an unbalanced microenvironment, are concerning with regards to their wider therapeutic applications. The activity of stem cells is mainly regulated by the anatomical niche; where they are placed during their clinical and therapeutic applications. Crosstalk between various niche signals maintains MSCs in homeostasis, in which the WNT signaling pathway plays vital roles. Several external or internal stimuli have been reported to interrupt the normal bioactivity of stem cells. The irreversible tissue loss that occurs during infection at the site of tissue grafting suggests an inhibitory effect mediated by microbial infections within MSC niches. In addition, MSC‑seeded tissue engineering success is difficult in various tissues, when sites of injury are under the effects of a severe infection despite the immunomodulatory properties of MSCs. In the present review, the current understanding of the way in which WNT signaling regulates MSC activity modification under physiological and pathological conditions was summarized. An effort was also made to illustrate parts of the underlying mechanism, including the inflammatory factors and their interactions with the regulatory WNT signaling pathway, aiming to promote the clinical translation of MSC‑based therapy.Diabetic nephropathy (DN) is a predominant cause of end‑stage renal disease. The impairment of the autophagy of human renal tubular epithelial cells (HK‑2 cells) is involved in the pathogenic mechanisms of DN. Sirtuin (Sirt)3 regulates the scavenging of damaged organelles and maintains energy balance. The present study aimed to examine the protective effects of Sirt3 on HK‑2 cells stimulated by high glucose (HG). HK‑2 cells were cultured in normal glucose (NG), HG or hyperosmotic medium. The viability of the HK‑2 cells was detected using a Cell Counting Kit‑8 assay. The expression and localization of Sirt3 were detected via immunofluorescence. Following transfection with an overexpression plasmid, the expression levels of key components in the Notch homolog 1 (Notch‑1)/hairy and enhancer of split‑1 (Hes‑1) pathway and those of the autophagy‑related proteins, Beclin‑1, LC‑3II and p62, were measured by western blot analysis and reverse transcription‑quantitative PCR (RT‑qPCR). As the Notch‑1/Hes‑1 pathway was iy, via the downregulation of Notch‑1/Hes‑1.Psoralen (PSO) exerts anti‑inflammatory pharmacological effects and plays an important role in a variety of inflammatory diseases. However, the effects of PSO with allergic rhinitis (AR) are yet to be reported. In the present study, an in vitro AR model was generated by inducing JME/CF15 human nasal epithelial cells with IL‑13, after which MTT was used to assess the cytotoxicity of PSO. The expression levels of inflammatory cytokines (granulocyte‑macrophage colony‑stimulating factor and Eotaxin) were determined by ELISA. Furthermore, the expression of inflammatory IL‑6 and ‑8, as well as mucin 5AC, was assessed by reverse transcription‑quantitative PCR and western blotting, and cellular reactive oxygen species were detected using a 2',7'‑dichlorodihydrofluorescein diacetate fluorescent probe. Western blotting was also used to detect the expression and phosphorylation of c‑Fos and c‑Jun in the activator protein 1 (AP‑1) pathway, as well as the expression of cystatin‑SN (CST1). PSO inhibited the inflammatory response and mucus production in IL‑13‑induced JME/CF15 cells. Furthermore, the levels of c‑Fos and c‑Jun phosphorylation in the AP‑1 pathway were decreased in IL‑13‑induced JME/CF15 cells following PSO treatment. The expression of pathway proteins was activated by the addition of PMA, an AP‑1 pathway activator, which concurrently reversed the inhibitory effects of PSO on the inflammatory response and mucus formation. The addition of an AP‑1 inhibitor (SP600125) further inhibited pathway activity, and IL‑13‑induced inflammation and mucus formation was restored. In conclusion, PSO regulates the expression of CST1 by inhibiting the AP‑1 pathway, thus suppressing the IL‑13‑induced inflammatory response and mucus production in nasal mucosal epithelial cells.Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the scratch-wound assay data shown in Fig. 3A and Transwell cell migration data shown in Figs. 3B and 6B were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to International Journal of Oncology, the Editor has decided that this paper should be retracted from the Journal. Selleck Proteasome inhibitor The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in International Journal of Oncology 48 541-550, 2016; DOI 10.3892/ijo.2015.3267].Studies have found that C‑C motif chemokine ligand 20 (CCL20)/C‑C motif chemokine receptor 6 (CCR6)/notch receptor 1 (Notch1) signaling serves an important role in various diseases, but its role and mechanism in ovarian cancer remains to be elucidated. The aim of the present study was to investigate the underlying mechanism of CCL20/CCR6/Notch1 signaling in paclitaxel (PTX) resistance of a CD44+CD117+ subgroup of cells in ovarian cancer. The CD44+CD117+ cells were isolated from SKOV3 cells, followed by determination of the PTX resistance and the CCR6/Notch1 axis. Notch1 was silenced in the CD44+CD117+ subgroup and these cells were treated with CCL20, followed by examination of PTX resistance and the CCR6/Notch1 axis. Furthermore, in nude mice, CD44+CD117+ and CD44‑CD117‑ cells were used to establish the xenograft model and cells were treated with PTX and/or CCL20, followed by proliferation, apoptosis, reactive oxygen species (ROS) and mechanism analyses. Higher expression levels of Oct4, CCR6, Notch1 and ATP binding cassette subfamily G member 1 (ABCG1), increased sphere formation ability, IC50 and proliferative ability, as well as lower ROS levels and apoptosis were observed in CD44+CD117+ cells compared with the CD44‑CD117‑ cells. It was found that CCL20 could significantly increase the expression levels of Oct4, CCR6, Notch1 and ABCG1, enhance the IC50, sphere formation ability and proliferation, as well as decrease the ROS and apoptosis levels in the CD44+CD117+ cells. However, Notch1 knockdown could markedly reverse these changes. Moreover, CCL20 could significantly increase the proliferation and expression levels of Oct4, CCR6, Notch1 and ABCG1 in the CD44+CD117+ groups compared with the CD44‑CD117‑ groups. After treatment with PTX, apoptosis and ROS levels were decreased in the CD44+CD117+ groups compared with the CD44‑CD117‑ groups. Collectively, the present results demonstrated that, via the Notch1 pathway, CCL20/CCR6 may promote the stemness and PTX resistance of CD44+CD117+ cells in ovarian cancer.