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In addition, pro‑apoptotic proteins were promoted following treatment of YD‑38 cells with lapiferin. Following the depletion ofP21 expression, lapiferin‑mediated inhibition of cell proliferation and enhancement of cell apoptosis were significantly reduced. These results indicated that lapiferin may exert potent antitumor effects on GSCC via regulation of P21; therefore, lapiferin may be considered a potential, natural therapeutic agent for the treatment of GSCC.Mitotic catastrophe, a cell death mechanism characterized by abnormal mitosis, has been regarded as a therapeutic approach for the development of anti‑cancer drug candidates. The aim of the present study was to investigate the potential effect of the ethanolic extract of Juniperus squamata (EEJS) on the occurrence of mitotic catastrophe in human oral cancer cell lines. The effect of EEJS on the occurrence of mitotic catastrophe was evaluated by measuring cytotoxicity, observing phase‑contrast or transmission electron microscope findings, evaluating the appearance of microtubule or chromosome abnormalities, and detecting the phosphorylation of histone H3 (Ser10). The apoptotic effect of EEJS was assessed by detecting cleaved PARP, analyzing the sub‑G1 population, Annexin V‑FITC/PI double staining, western blot analysis, and the transient transfection of myeloid cell leukemia‑1 (Mcl‑1) overexpression vectors. EEJS treatment was effective in inhibiting cell proliferation in human oral cancer cell lines. EEJS resulted in the enrichment of enlarged multinucleated cells, the disturbance of microtubule formation, and increased phosphorylation of histone H3 (Ser10), which demonstrates the occurrence of mitotic catastrophe. Additionally, the multinucleated cells underwent apoptotic cell death in a cell context‑dependent manner, which was associated with the reduction of Mcl‑1 protein levels. Findings of the present study indicate that EEJS could be effective for treating human oral cancer by promoting mitotic catastrophe linked to apoptotic cell death.The phenotypes and mechanisms underlying the proliferation and migration of vascular smooth muscle cells (VSMCs) induced by oleic acid (OA) are not completely understood. Therefore, the aim of the present study was to further elucidate the effects of OA on the proliferation and migration of VSMCs. Using A7r5 cells, the hepatocyte growth factor (HGF) inhibitor PHA665752 and the p38 MAPK inhibitor SB203580 were utilized, and Cell Counting Kit‑8 (CCK‑8) assays, Transwell assays, flow cytometry, ELISAs, western blotting and reverse transcription‑quantitative PCR (RT‑qPCR) were conducted to assess the effects of OA. CCK‑8 assays indicated that OA promoted (at 5 and 50 µmol/l) or inhibited (at 800 µmol/l) A7r5 cell proliferation in a time‑ and concentration‑dependent manner (P less then 0.05). Transwell assays revealed that OA also promoted (at 50 µmol/l) or inhibited (at 800 µmol/l) A7r5 cell migration (P less then 0.05). Moreover, cell‑cycle analysis identified that 50 µmol/l OA reduced the cellular population in and the p38 MAPK pathway. Moreover, the proliferation and migration of VSMCs induced by OA was associated with increased expression levels of HGF and p‑p38. Taken together, OA, HGF and p38 MAPK may be potential therapeutic targets for the treatment of atherosclerosis.Following the publication of the above paper, a concerned reader drew to the Editor's attention that several figures (Figs. 3‑8 inclusive) contained apparent anomalies, including repeated patternings of data within the same figure panels. After having conducted an independent investigation in the Editorial Office, the Editor of Molecular Medicine Reports has determined that the above paper should be retracted from the Journal on account of a lack of confidence concerning the originality and the authenticity of the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office never received any reply. selleck chemical The Editor regrets any inconvenience that has been caused to the readership of the Journal. [the original article was published on Molecular Medicine Reports 17 1035‑1040, 2018; DOI 10.3892/mmr.2017.7977].Pulmonary arterial hypertension (PAH), is a chronic and progressive disorder characterized by pulmonary vascular remodeling, including endothelial cell dysfunction and inflammation. MicroRNAs (miRNAs or miRs) play an important role in the development of PAH. In addition, fibroblast growth factor 21 (FGF21) has been found to have marked anti-dysfunction and anti‑inflammatory properties. Therefore, the present study aimed to investigate the latent effects of FGF21 against PAH through the miR‑27b/peroxisome proliferator‑activated receptor γ (PPARγ) axis. Human pulmonary arterial endothelial cells (HPAECs) subjected to hypoxia were used as PAH models. The results revealed that PPARγ expression was downregulated and miR‑27b expression was upregulated in the HPAECs exposed to hypoxia. Luciferase assay suggested that PPARγ was a target gene of miR‑27b. Furthermore, miR‑27b inhibited the expression of the PPARγ gene, thereby aggravating hypoxia‑induced HPAEC dysfunction. Moreover, miR‑27b activated the nuclear factor‑κB signaling pathway and the expression of inflammatory factors [interleukin (IL)‑1β, IL‑6 and tumor necrosis factor‑α] by targeting PPARγ. 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. 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.
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