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.

The ring finger protein 8 (RNF8), a key component of protein complex crucial for DNA-damage response, consists of a forkhead-associated (FHA) domain and a really interesting new gene (RING) domain that enables it to function as an E3 ubiquitin ligase. However, the biological functions of RNF8 in estrogen receptor α (ERα)-positive breast cancer and underlying mechanisms have not been fully defined. Here, we have explored RNF8 as an associated partner of ERα in breast cancer cells, and co-activates ERα-mediated transactivation. Accordingly, RNF8 depletion inhibits the expression of endogenous ERα target genes. Interestingly, our results have demonstrated that RNF8 increases ERα stability at least partially if not all via triggering ERα monoubiquitination. RNF8 functionally promotes breast cancer cell proliferation. RNF8 is highly expressed in clinical breast cancer samples and the expression of RNF8 positively correlates with that of ERα. Up-regulation of ERα-induced transactivation by RNF8 might contribute to the promotion of breast cancer progression by allowing enhancement of ERα target gene expression. Our study describes RNF8 as a co-activator of ERα increases ERα stability via post-transcriptional pathway, and provides a new insight into mechanisms for RNF8 to promote cell growth of ERα-positive breast cancer.

Stem cells transplantation is a promising therapy strategy for accelerating periodontal regeneration and reconstruction. Genetic modification could induce stem cells directional differentiation to facilitate recovery of physiological functions. In this study, we investigated the role and mechanism of miR-22 on human periodontal ligament stem cells (PDLSCs). First, a cellular model of osteogenic differentiation was first established by osteogenic inductive cocktail. Real-time PCR determined that expression of miR-22 was significantly increased during PDLSCs osteogenic differentiation. Alizirin red staining showed that overexpression of miR-22 in PDLSCs induced better mineralized nodule formation. Real-time PCR and Western blot further confirmed up-regulation of osteogenic genes Runx2 and OPN in miR-22-overexpressing PDLSCs. Conversely, inhibition of miR-22 delayed the process of PDLSCs osteogenic differentiation. Furthermore, Histone deacetylase 6 (HDAC6) was identified as a target gene of miR-22. Overexpression of miR-22 not only reduced the luciferase activity of the reporter containing the 3' untranslated region of HDAC6 mRNA, but also suppressed the endogenous protein expression of HDAC6. Rescue experiment showed that the promotion role of miR-22 in osteogenic differentiation could be relieved by overexpression of HDAC6. Meanwhile, overexpression of HDAC6 alone could also delay the osteogenic differentiation process. The results demonstrated that miR-22 promoted PDLSCs osteogenic differentiation by inhibiting HDAC6 expression, suggesting that miR-22 might be developed as a target of genetic modified stem cells therapy for periodontal diseases. J. Cell. Biochem. 118: 1653-1658, 2017. © 2017 Wiley Periodicals, Inc.

The aim of the present study was to compare the outcomes of superficial parotidectomy (SP) and partial superficial parotidectomy (PSP) in treating benign parotid tumors. Individuals who had undergone SP or PSP between 2005 and 2008 were enrolled, the medical records were reviewed, and a questionnaire was created and mailed to the patients. For the statistical analysis, χ2 and non-parametric Mann-Whitney tests were used to analyze the variables. In total, 320 patients were included in the present study. Within the PSP group, immediate facial nerve weakness occurred in six patients (7.6%), and Frey’s syndrome occurred in five (6.3%). Despite this, facial nerve function recovered fully during the follow-up, and recurrence was not identified. Within the SP group, Frey’s syndrome occurred in 38 patients (15.8%), immediate facial nerve weakness in 55 patients (22.8%) and permanent facial nerve dysfunction in two patients (0.8%). However, no recurrence was evident. In total, 216 (67.5%) patients returned the questionnaire. Those with PSP demonstrated improved scores in the domains of appearance, facial contours, facial nerve function and Frey’s syndrome. Compared with SP, PSP not only decreased the incidence of Frey’s syndrome and transient facial nerve weakness, but also improved quality of life outcomes and guaranteed a low recurrence rate.

No abstract