ABSTRACT
[This retracts the article DOI: 10.3892/etm.2017.4998.].
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[This retracts the article DOI: 10.3892/etm.2014.1708.].
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AIM: The mediating role of emotional disorders between conflict management styles and work engagement was explored based on constructing structural equation models in paediatric nurses. DESIGN: A cross-sectional study. METHODS: According to a cross-sectional survey, 300 paediatric nurses were selected from three tertiary hospitals (Chang sha, China), the data were collected using demographic questionnaires, the Rahim Organizational Conflict Inventory-II, Depression, Anxiety and Stress Scales and the Utrecht Work Engagement Scale. The Structural Equation Model was employed to investigate the mediating role of emotional disorders between conflict management styles and work engagement. RESULTS: Among conflict management styles, emotional disorders and work engagement, the associations were all significant (p < .05). In the mediation models, emotional disorders partially mediate the relationships between conflict management styles and work engagement (indirect effect 0.095, p < .01; direct effect -0.330, p < .01; total effect -0.330, p < .01) and between conflict management styles and work engagement (indirect effect 0.095, p < .01; direct effect 0.329, p < .01; total effect 0.424, p < .01).
Subject(s)
Nurses, Pediatric , Work Engagement , Child , Humans , Cross-Sectional Studies , China , Surveys and QuestionnairesABSTRACT
[This retracts the article DOI: 10.3892/etm.2017.4595.].
ABSTRACT
MicroRNA (miR)-124 has been implicated in malignant melanoma (MM). However, the detailed regulatory mechanism of miR-124 in the malignant phenotypes of MM cells has remained largely elusive. A total of 68 pairs of MM tissues and adjacent tissues were collected. Reverse-transcription quantitative polymerase chain reaction was used to examine the mRNA expression of versican as well as the expression of miR-124, and the protein expression of versican was assessed by western blot analysis. MTT, wound healing and Transwell assays were used to determine cell proliferation, migration and invasion, respectively. A bioinformatics analysis and a luciferase reporter assay were used to confirm the targeting association between miR-124 and versican. miR-124 was significantly downregulated in MM tissues compared with that in adjacent non-tumorous tissues, and decreased expression of miR-124 was associated with increased tumor thickness, advanced clinical stage and node metastasis of MM. Furthermore, the expression levels of miR-124 were also reduced in MM cell lines compared with normal human skin HACAT cells. Forced overexpression of miR-124 caused a significant reduction in the proliferation, migration and invasion of MM A375 cells. Versican was significantly upregulated in MM tissues and cell lines, and was identified as a novel target of miR-124 in A375 cells using a luciferase reporter gene assay, and miR-124 was revealed to negatively regulate the protein expression of versican in A375 cells. Overexpression of versican impaired the suppressive effects of miR-124 on the proliferation, migration and invasion of A375 cells. In conclusion, miR-124 inhibited the malignant phenotypes of MM cells at least partly via inhibition of versican. Therefore, the miR-124/versican axis may be used as a promising therapeutic target for inhibiting MM growth and metastasis.
ABSTRACT
MicroRNA (miR) are a class of small non-coding RNA that are able to inhibit gene expression by directly binding to the 3' untranslated region (UTR) of their target mRNA and thus promote translational repression or mRNA degradation. Recently, miR-9 was reported to have a suppressive role in malignant melanoma; however, the underlying mechanism remains largely unclear. In the present study, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting were used to examine the mRNA and protein expression levels in malignant melanoma tissues and cell lines. The MTT assay and wound healing assay were used to examine the cell viability, proliferation and migratory capacities. Bioinformatics prediction and luciferase reporter assay were performed to investigate the relationship between miR-9 and its potential target gene. The present data revealed that miR-9 expression was significantly downregulated in malignant melanoma tissues when compared with their matched adjacent non-tumor tissues. Furthermore, the expression levels of miR-9 were reduced in malignant melanoma cell lines when compared with human normal skin HACAT cells. Moreover, the ectopic expression of miR-9 significantly suppressed the proliferation and migration of malignant melanoma cells, accompanied with a remarkable decrease in the protein expression levels of sirtuin 1 (SIRT1), which were markedly upregulated in malignant melanoma tissues and cell lines. Additionally, restoration of SIRT1 reversed the suppressive effects of miR-9 on the proliferation and migration of malignant melanoma cells. Luciferase reporter assay data further identified SIRT1 as a direct target gene of miR-9. To conclude, the present findings indicate that miR-9 has a suppressive role in malignant melanoma cell viability and migration, at least in part, via directly inhibiting the protein expression of its target gene, SIRT1. Therefore, miR-9 may serve as a potential candidate for the treatment of malignant melanoma.
ABSTRACT
MicroRNA (miR)-203 has been demonstrated to function as a suppressor in tumorigenesis. Recently, miR-203 was reported to play a role in malignant melanoma (MM); however, the detailed function of miR-203 in MM remains unclear. In the present study, the expression of miR-203 was shown to be significantly downregulated in MM tissues when compared with normal adjacent tissues. Based on a bioinformatic prediction, versican was further identified as a novel target of miR-203, and the expression of versican was markedly increased in MM tissues. Inhibition of miR-203 increased the protein expression of versican, while upregulation of miR-203 inhibited the protein expression of versican in MM A375 cells. In addition, the upregulation of versican significantly promoted A375 cell migration; however, upregulation of miR-203 suppressed A375 cell migration. The present study further investigated whether miR-203 was involved in versican-mediated A375 cell migration, and the results indicated that upregulation of miR-203 significantly inhibited A375 cell migration, which was impaired by overexpression of versican. These observations indicated that versican functions as a downstream effector in miR-203-mediated MM cell migration. Therefore, the results demonstrated that miR-203 exhibited an inhibitory effect on MM cell migration via directly targeting versican, thus, may become an effective inhibitor for MM metastasis.
