Thyroid cancer, the most common primary endocrine malignancy in adult, imperatively requires new therapeutic studies that could target the molecular regulatory mechanism. Even though emerging evidence showed that long noncoding RNAs (Lnc-RNAs) are involved in different biological characteristic of malignant tumor, such as cell growth and apoptosis as well as cancer progression and metastasis. Limited data are available on the function of Lnc-RNAs in thyroid cancer invasion and metastasis. Among the 5 tested lnc-RNAs , the present study demonstrates that MEG3 was significantly down-regulated in papillary thyroid carcinoma (PTC) tissues with lymph-node metastasis than in primary thyroid cancer. Moreover, the down- regulated MEG3 was associated with lymph-node metastasis. Over-expression of MEG3 could strongly inhibit the cell migration and invasion in TPC-1 and HTH83 thyroid cancer cell lines. In addition, we also showed that Rac1 was negatively regulated by lncRNA-MEG3 at the posttranscriptional level, via a specific target site within the 3΄UTR by dual luciferase reporter assay. The expression of Rac1 was inversely correlated with lncRNA-MEG3 expression in PTC tissues. Thus, this study suggests that MEG3 acts as novel suppressor of migration and invasion by targeting Rac1 gene.

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.

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.

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).