miR-362-3p inhibited the invasion and metastasis of oral squamous cell carcinoma cells by targeting the regulation of pituitary tumor-transforming gene 1.

OBJECTIVES: This study aimed to explore the effect of pituitary tumor-transforming gene 1 (PTT-G1) on the invasion and proliferation of oral squamous cell carcinoma (OSCC) cell lines under the action of miR-362-3p. METHODS: The bioinformatics online database was used to query the expression of PTTG1 in head and neck squamous cell carcinoma (HNSCC). The expression of PTTG1 in the Cal-27, HN-30, and HOK cell lines was detected by Western blot. A wound-healing assay was used to determine the effect of PTTG1 on the migration ability of the OSCC cells. The Transwell assay was used to examine the changes in cell-invasion ability. 5-ethynyl-2'-deoxyuridine (EdU) cell-proliferation assay was used to detect changes in cell-proliferation ability. Bioinformatics approach predicted the upstream miRNA of PTTG1. The targeting relationship between miR-362-3p and PTTG1 was examined by the dual luciferase assay, and quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expression of miRNA in OSCC tissues. RESULTS: The ENCORI database showed that PTTG1 expression was up-regulated in OSCC tissues. Western blot confirmed that PTTG1 expression was up-regulated in Cal-27 and HN-30 cells than HOK cells. PTTG1 knockout can inhibit the migration, invasion, and proliferation of Cal-27 and HN-30 cells (P<0.05). Bioinformatics prediction websites predicted that the upstream miRNA of PTTG1 was miR-362-3p, and PTTG1 can bind to miR-362-3p. Results of qRT-PCR showed that miR-362-3p expression was downregulated in OSCC tissues compared with normal tissue (P<0.05). Transwell and EdU experiments confirmed that miR-362-3p knockdown can promote the invasion and proliferation of Cal-27 and HN-30 after PTTG1 knockdown. CONCLUSIONS: miR-362-3p can inhibit the invasion and proliferation of Cal-27 and HN-30 cells by targeting PTTG1.

A hierarchical nanostructural coating of amorphous silicon nitride on polyetheretherketone with antibacterial activity and promoting responses of rBMSCs for orthopedic applications.

Silicon nitride (SN) with good osteoconductivity has been introduced as an implantable biomaterial for joint replacement and interbody fusion devices. In this study, SN was coated on a polyetheretherketone (PEEK) surface by inductively coupled plasma-enhanced chemical vapor deposition (ICPECVD). The results showed that a dense coating (thickness of about 500 nm) of amorphous SN was closely combined with a PEEK substrate (PKSN) with a binding strength of 6.88 N. In addition, the coating surface showed hierarchical nanostructures containing many spherical bulges (sizes about 150 nm), which were composed of many small humps (sizes about 10 nm). Moreover, the roughness, hydrophilicity, surface energy, surface charge and adsorption of bovine serum albumin (BSA) of PKSN were obviously higher than those of PEEK. After immersion into simulated body fluid (SBF), the Si ions were gradually released from PKSN into SBF and a weak alkaline environment was created. Antibacterial experiments showed that PKSN exhibited a greater antibacterial activity than that of PEEK. Moreover, compared with PEEK, PKSN significantly promoted adhesion, proliferation, differentiation and expression of osteogenic related genes of the rat bone marrow stromal cells (rBMSCs). In conclusion, the SN coating of PKSN with hierarchical nanostructures exhibited excellent antibacterial activity and cytocompatibility, which would make it a great candidate for orthopedic applications.