Hartmannhermann2165

In addition, the expression of miR‑27b decreased following treatment of the hypoxia‑exposed HPAECs with FGF21. Furthermore, FGF21 alleviated hypoxia‑induced HPAEC dysfunction and inflammation by inhibiting miR‑27b expression and thereby promoting PPARγ expression. On the whole, the findings of the present study suggest that FGF21 may serve as a therapeutic target for managing PAH through the miR‑27b‑mediated PPARγ pathway.After the publication of the article, and also the publication of a Corrigendum (see doi 10.3892/or.2020.7744), there are further errors in the published paper that the authors wish to correct in a subsequent corrigendum. In the printed version of Fig. 5, the "NC" images were mistakenly presented in the data panels showing the results of the TCA8113 and TSCCA invasion assay experiments. Furthermore, in Fig. GSK1904529A manufacturer 4A and 6A, the β‑actin control bands were erroneously selected for these figures. The corrected versions of Figs. 4, 5 and 6 are shown opposite and on the next page, incorporating the correct data for Figs. 4A, 5 and 6A. These further corrections do not affect the results and conclusions of this work. The authors all agree to this Corrigendum, and are grateful to the Editor of Oncology Reports for allowing them to have the opportunity to correct these additional errors. Lastly, the authors apologize to the readership for any inconvenience these errors may have caused. [the original article was published in Oncology Reports 39 1853‑1859, 2018; DOI 10.3892/or.2018.6231].Chemoresistance is the main cause of poor prognosis in colorectal cancer (CRC). Nicotinamide N‑methyltransferase (NNMT) is a metabolic enzyme that is upregulated in various tumor types. It has been reported that NNMT inhibits apoptosis and enhances resistance to 5‑fluorouracil (5‑Fu) via inhibition of the apoptosis signal regulating kinase 1 (ASK1)‑p38 MAPK pathway in CRC cells. A natural product library was screened, and it was found that vanillin, also known as 4‑hydroxy‑3‑methoxybenzaldehyde, a plant secondary metabolite found in several essential plant oils, mainly Vanilla planifolia, Vanilla tahitensis, and Vanilla pompon, may be a promising anticancer compound targeted to NNMT. The aim of the present study was to explore the effect of vanillin on promoting apoptosis and attenuating NNMT‑induced resistance to 5‑Fu in CRC. Lentiviral vectors of short hairpin RNA and small interfering RNA were transfected into HT‑29 cells to construct NNMT‑knockdown HT‑29 cell lines. Vectors containing an open reading frame of NNMT were stably transfected into SW480 cells to induce NNMT overexpression in SW480 cell lines. Vanillin was found to inhibit the mRNA and protein expression levels of NNMT following the inhibition of NNMT activity in HT‑29 cell lines. Vanillin was able to reverse NNMT‑induced increased cell proliferation, decreased cell apoptosis and resistance to 5‑Fu by inhibiting NNMT expression. Furthermore, it increased cell apoptosis by activating the ASK1‑p38 MAPK pathway, which could be inhibited by NNMT. In addition, vanillin increased cell apoptosis by promoting mitochondrial damage and reactive oxygen species. In vivo, the combination of vanillin with 5‑Fu yielded a notable synergy in inhibiting tumor growth and inducing apoptosis. Considering that vanillin is an important flavor and aromatic component used in foods worldwide, vanillin is deemed to be a promising anticancer candidate by inhibiting NNMT and may attenuate NNMT‑induced resistance to 5‑Fu in human CRC therapy with few side effects.The current study aimed to evaluate the accuracy of diffusion‑weighted imaging and morphological aspects at 3 Tesla (T) and 1.5T MRI for diagnosing metastatic lymph nodes (LN) in cervical cancer. A retrospective study was conducted at the Barretos Cancer Hospital. link2 A total of 45 patients with cervical cancer who underwent MRI examination and pelvic and/or para‑aortic lymphadenectomy as part of surgical procedure were included. Data regarding LN images included size (short‑axis diameters), morphology (usual, rounded or amorphous), appearance (homogeneous or heterogeneous), limits (regular, irregular or imprecise), presence or absence of necrosis, diffusion (normal or greater restriction than expected for normal tissue) and aspect (suspected, undetermined or normal). These findings were compared with histopathological results. According to histology results, among the 45 patients, 14 (31.1%) LNs were tested positive for metastasis and 31 (68.9%) LNs were tested negative. A total of 41 metastatic positive LNs were detected from a total of 976 resected nodes. Twelve patients from the 45 (26.7%) had LN classified as metastatic by histology and suspected by MRI, 26 (57.8%) as negative in both evaluations, 2 (4.4%) as positive by histology and negative by MRI and five (11.1%) as negative by histology and positive by MRI. Based on these results, sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV) and accuracy were 85.7, 83.9, 70.6, 92.9 and 84.4%, respectively. The Cohen's κ test exposed a general outcome of 0.657 (P10 mm, T2 hypointensity, rounded morphology and greater restriction than expected for normal tissues. If these four characteristics are present in MRI, histological evaluation is likely to reveal positive lymph node metastasis.Due to the lack of specific symptoms in early thymic epithelial tumours (TETs), patients are mostly in the advanced stage at the time of presentation. The aim of the present study was to explore the mechanism by which the long noncoding RNA (lncRNA) LOXL1‑AS1 affects thymoma and thymic carcinoma progression by targeting the miR‑525‑5p‑HSPA9 axis. Bioinformatics was used to analyse the process of LOXL1‑AS1 targeting miR‑525‑5p‑HSPA9 and its expression characteristics in TET. The relationships between LOXL1‑AS1, miR‑525‑5p, HSPA9 and prognosis were analysed. The dual luciferase reporter assay was applied to verify targeting. The gene was knocked down or overexpressed by plasmid transfection. Cell counting kit 8 (CCK‑8) assay, flow cytometry and Transwell assay were used to detect cell viability, apoptosis and invasion ability, respectively. Proteins and RNAs were examined by western blot analysis and qPCR, respectively. A tumour‑burdened assay was used to perform in vivo verification. LOXL1‑AS1 and HSPA9 were ond invasion and inhibiting apoptosis of thymoma and thymic carcinoma cells.Long non‑coding RNAs (lncRNAs) play a crucial role in cancer development. However, researchers have yet to identify the underlying association between lncRNAs and ovarian cancer (OC). The aim of the present study was to examine the effect of lncRNA RHPN1‑AS1 (RHPN1‑AS1) on OC cells and tissues. Reverse transcriptase‑quantitative PCR (RT‑qPCR) was utilized to quantify RHPN1‑AS1, miR‑485‑5p, and TPX2 mRNA expression in samples with OC. Luciferase‑reporter assay, RNA immunoprecipitation (RIP) assay, and RNA pull‑down assay were then employed to validate the target relationship among RHPN1‑AS1, miR‑485‑5p and TPX2. Cell Counting Kit‑8, BrdU, wound‑healing, cell‑adhesion, and flow cytometry assays were also employed to assess cell viability, proliferation, migration, adhesion and apoptosis, respectively, in SKOV3 and OVCAR3 cell lines. link3 Findings revealed that RHPN1‑AS1 demonstrated a higher expression level in OC cell lines and tissues. In addition, RHPN1‑AS1 enhanced the adhesion, proliferation and migration of OC cell lines but decreased apoptosis of OC cells. It was also observed that the relationship between RHPN1‑AS1 and miR‑485‑5p was negative and that RHPN1‑AS1 could sponge miR‑485‑5p to regulate the proliferation, apoptosis, adhesion, and migration abilities of OC cells. Moreover, TPX2 was targeted by miR‑485‑5p and was significantly overexpressed in OC cell lines and tissues. Experimental investigations also revealed that TPX2 promoted the proliferation, adhesion, and migration of OC cells but suppressed the apoptosis of SKOV3 and OVCAR3 cells. In summary, RHPN1‑AS1 played a tumor promotive role by sponging miR‑485‑5p to increase TPX2 expression in OC tumorigenesis.Overexpression of ETS‑homologous factor (EHF) in non‑small cell lung cancer (NSCLC) is associated with poor patient prognosis. To explore the mechanism of the effect of EHF in NSCLC, EHF expression was examined in NSCLC and its role in cell proliferation, invasion, cell cycle, and apoptosis of NSCLC cells was evaluated by overexpressing EHF and/or knocking down EHF expression in NSCLC cells in vitro and in cancer cell grafted mice in vivo. The results revealed that the knockdown of EHF expression in NSCLC with siRNA significantly inhibited cell proliferation and invasion, arrested the cell cycle at the G0/G1 phase, and induced apoptosis, whereas overexpression of EHF in NSCLC promoted cell proliferation, tumor growth, and cancer cell migration in vitro. The in vivo experiments demonstrated that siRNA‑mediated downregulation of EHF expression in NSCLC cells significantly suppressed tumor growth in xenografted nude mice as compared to cancer progression in the mice grafted with NSCLC cells transfected with non‑specific control siRNA. The biochemical analyses revealed that EHF promoted NSCLC growth by regulating the transcription of Erb‑B2 receptor tyrosine kinase 2/3 (ERBB2, ERBB3) and mesenchymal‑epithelial transition (MET) factor tyrosine kinase receptors and modulating the AKT and ERK signaling pathways in the NSCLC cells. The present findings indicated that EHF could be used as a prognostic marker for NSCLC, and tyrosine kinase receptors of ERBB2, ERBB3 and MET could be drug targets for NSCLC treatment.Nowadays, metabolic syndromes are emerging as global epidemics, whose incidence are increasing annually. However, the efficacy of therapy does not increase proportionately with the increased morbidity. Type 2 diabetes mellitus (T2DM) and non‑alcoholic fatty liver disease (NAFLD) are two common metabolic syndromes that are closely associated. The pathogenic mechanisms of T2DM and NAFLD have been studied, and it was revealed that insulin resistance, hyperglycemia, hepatic lipid accumulation and inflammation markedly contribute to the development of these two diseases. The 2‑series prostaglandins (PGs), a subgroup of eicosanoids, including PGD2, PGE2, PGF2α and PGI2, are converted from arachidonic acid catalyzed by the rate‑limiting enzymes cyclooxygenases (COXs). Considering their wide distribution in almost every tissue, 2‑series PG pathways exert complex and interlinked effects in mediating pancreatic β‑cell function and proliferation, insulin sensitivity, fat accumulation and lipolysis, as well as inflammatory processes. Previous studies have revealed that metabolic disturbances, such as hyperglycemia and hyperlipidemia, can be improved by treatment with COX inhibitors. At present, an accumulating number of studies have focused on the roles of 2‑series PGs and their metabolites in the pathogenesis of metabolic syndromes, particularly T2DM and NAFLD. In the present review, the role of 2‑series PGs in the highly intertwined pathogenic mechanisms of T2DM and NAFLD was discussed, and important therapeutic strategies based on targeting 2‑series PG pathways in T2DM and NAFLD treatment were provided.