LncRNA FALEC promotes proliferation, migration, and invasion of PTC cells through regulating Wnt/ß-catenin signaling pathway.

OBJECTIVE: The aim of this study was to explore the expression of long non-coding ribonucleic acid (lncRNA) FALEC (hereinafter referred to as FALEC) in papillary thyroid carcinoma (PTC) and its effects on the proliferation, invasion, and metastasis of PTC cells. PATIENTS AND METHODS: Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) was performed to measure the expression level of FALEC in 48 cases of PTC tissues and cells. The small interfering (si)-FALEC was synthesized and transfected into PTC cells. Interference efficiency was confirmed via qRT-PCR assay. Subsequently, the effect of FALEC on the proliferation of PTC cells was determined by cell counting kit-8 (CCK-8) assay. Wound healing and transwell assays were conducted to detect the effects of FALEC on the invasion, migration, and metastasis of PTC cells. Additionally, changes in the protein expression of Wnt/ß-catenin signaling pathway molecular markers was detected via Western blotting. RESULTS: The expression level of FALEC was significantly higher in PTC tissues than that of adjacent normal tissues. FALEC expression was significantly up-regulated in PTC cell lines, as well. CCK-8 assay revealed that the proliferation ability of PTC cells was remarkably weakened after down-regulation of FALEC in vitro. Wound healing and transwell assays demonstrated that, compared with si-normal control (NC) group, the migration and invasion capabilities declined significantly in si-FALEC group. Furthermore, the Western blotting analysis indicated that the expression of Wnt/ß-catenin signaling pathway molecular markers was changed after the interference in FALEC expression. CONCLUSIONS: FALEC expression was up-regulated in PTC tissues and cell lines. Highly expressed FALEC facilitated the proliferation, migration, and invasion of PTC by regulating the Wnt/ß-catenin signaling pathway.

Diagnostic and prognostic implications of serum miR-101 in osteosarcoma.

Blood-circulating microRNAs (miRNAs) have been reported to be used as potential biomarkers in various cancers. MiR-101 has been found to act as a tumor suppressor in many tumor types, but little is known for osteosarcoma. The purpose of this study was to investigate miR-101 expression in osteosarcoma patients and assess its correlation with clinical features and prognosis. Serum samples from 152 osteosarcoma patients and 70 healthy controls were detected using quantitative reverse-transcription polymerase chain reaction (qRT-PCR). The data showed that miR-101 expression levels were remarkably underexpressed in serum samples from osteosarcoma patients compared to controls, and the post-treatment serum miR-101 expression was significantly higher than that in the pre-treatment expression. Low serum miR-101 expression was positively associated with advanced clinical stage and distant metastasis. Receiver operating characteristic (ROC) curve analysis showed that serum miR-101 could serve as a useful marker for osteosarcoma diagnosis, with a high sensitivity and specificity. Moreover, patients with high miR-101 expression had longer overall survival and recurrence free survival than those with low miR-101 expression. In addition, both univariate and multivariate analyses showed that serum miR-101 downregulation was associated with shorter overall survival and recurrence free survival. Our present results implicated serum miR-101 might be a useful biomarker for the clinical diagnosis and prognosis of osteosarcoma.

Stacking fault-mediated ultrastrong nanocrystalline Ti thin films.

In this work, we prepared nanocrystalline (NC) Ti thin films with abundant stacking faults (SFs), which were created via partial dislocations emitted from grain boundaries and which were insensitive to grain sizes. By employing the nanoindentation test, we investigated the effects of SFs and grain sizes on the strength of NC Ti films at room temperature. The high density of SFs significantly strengthens NC Ti films, via dislocation-SF interactions associated with the reported highest Hall-Petch slope of ∼20 GPa  nm1/2, to an ultrahigh strength of ∼4.4 GPa, approaching ∼50% of its ideal strength.

Biological characteristics of staphylococcal enterotoxin Q and its potential risk for food poisoning.

AIMS: To elucidate the biological characteristics and stability of a newly identified staphylococcal enterotoxin Q (SEQ) against heating and digestive enzymes and to evaluate the risk of seq-harbouring Staphylococcus aureus in food poisoning. METHODS AND RESULTS: Purified SEQ was treated with heating, pepsin and trypsin which are related to food cooking, stomach and intestine conditions, respectively. Superantigenic activity of SEQ was assessed by determining the ability of IL-2 induction in mouse spleen cells. The emetic activity of SEQ was assessed using house musk shrew, a small emetic animal model. The results revealed that SEQ exhibits a remarkable resistance to heat treatment and pepsin digestion and has significant superantigenic and emetic activities. Furthermore, a sandwich ELISA for detection of SEQ production was developed, and the results showed that seq-harboring S. aureus isolates produce a large amount of SEQ. CONCLUSIONS: The newly identified SEQ had remarkable stability to heat treatment and digestive enzyme degradation and exhibited significant superantigenic and emetic activities. In addition, seq-harbouring S. aureus isolated from food poisoning outbreaks produced a large amount of SEQ, suggesting that seq-harbouring S. aureus could potentially be a hazard for food safety. SIGNIFICANCE AND IMPACT OF THE STUDY: This study found, for the first time, that SEQ, a nonclassical SE, had remarkable stability to heat treatment and enzyme degradation and exhibited significant emetic activity, indicating that SEQ is a high-risk toxin in food poisoning.

Incidence of mononeuropathy in rats is influenced by pre-emptive alteration of spinal excitability.

Both clinical and experimental data support the notion that the development of neuropathic pain is related to the state of excitability at the time of nerve injury. The present study was performed to investigate whether altering spinal excitability immediately before creation of a chronic constriction nerve injury in rats can influence the incidence of tactile hypersensitivity ('allodynia') by using pre-emptive: (1) intrathecal injection of a GABAB agonist or antagonists; (2) intrathecal lidocaine; or (3) C-fibre activation by electric stimulation. The incidence of tactile hypersensitivity was significantly reduced by the GABA(B) agonist baclofen while it was markedly enhanced by the administration of the GABA(B) antagonists 5-AVA and CGP 55845, as well as by C-fibre stimulation. Intrathecal administration of lidocaine did not influence the incidence of hypersensitivity. The results suggest that GABAergic mechanisms play an important role in the development of tactile hypersensitivity, and suggest that GABA(B) receptor agonists may be used as pre-emptive treatment to prevent the development of postinjury neuropathic pain.