Construction and performance evaluation of a sustained release implant material polyetheretherketone with antibacterial properties.

OBJECTIVE: This study aimed to construct a tightly binding antibiotic sustained release system on the polyetheretherketone (PEEK) surface and investigate the cellular activity and antibacterial properties of the new oral implant materials. METHODS: Low-temperature argon plasma under certain parameters was used to prepare P-PEEK with nano-topology, and chemical deposition technology was adopted to form a polydopamine (PDA) coating on the PEEK surface to build a biological binding platform, PDA/P-PEEK. Subsequently, vancomycin gelatin nanoparticles (Van-GNPs) were prepared by two-step desolvation method. Finally, Van-GNPs were combined with PEEK implant material surface to form a new composite material, Van-GNPs/PEEK. scanning electron microscope (SEM), atomic force microscope (AFM), energy dispersive spectrometer (EDS), and contact angle tester were used to comprehensively characterize the materials. The in vitro release test of Van was performed by dynamic dialysis with ultraviolet spectrophotometer. The cell cytotoxicity and adhesion tests were studied by mouse embryonic osteoblasts. The antibacterial properties were evaluated by bacterial adhesion test, plate colony counting, and antimicrobial ring test with Staphylococcus aureus and Streptococcus mutans. RESULTS: PEEK was treated with low-temperature argon plasma and attached to PDA to form a biological binding platform. The synthesized Van-GNPs were smooth, round, with uniform particle size distribution, and bound to PEEK to form a new composite material, which can release Van constantly. Cell experiments showed that Van-GNPs/PEEK had no cytotoxicity and had good interaction with osteoblasts. Bacterial experiments showed that surface conjugation with Van-GNPs could significantly improve the antibacterial performance of PEEK against S. aureus and S. mutans. SIGNIFICANCE: This study demonstrated that Van-GNPs/PEEK have good cellular compatibility and autonomous antibacterial properties, which provide a theoretical basis for the wide application of PEEK in the field of stomatology.

C-reactive protein promotes tongue squamous cell carcinoma chemoresistance by inhibiting the activation of caspase-3/9 via the CD64/AKT/mTOR pathway.

Recent studies have shown that C-reactive protein (CRP) participates in multiple types of cancer development. Here, the aim of this study was to investigate the role of CRP in tongue squamous cell carcinoma (TSCC) chemoresistance. Immunohistochemical staining showed that CRP expression was upregulated in TSCC tissues from cisplatin-resistant patients compared with that in cisplatin-sensitive TSCC samples. The CRP expression level was positively correlated with that of the drug-resistant marker MDR1. Moreover, functional experiments showed that CRP increased cell viability and decreased cisplatin-induced apoptosis. CRP also increased the expression levels of MDR1 and Bcl-2 and decreased the expression level of Bax. Furthermore, CRP decreased the activity of caspase-3. Mechanistically, CRP could bind to Fcγ receptor I (FcγRI, also known as CD64) and activate the AKT/mTOR pathway to inhibit the activation of caspase-3/9, as shown by co-immunoprecipitation (Co-IP) assay and western blotting assays. In addition, CRP promoted tumour growth and decreased cleaved caspase-3/9 expression in BALB/c nude mice. Taken together, our findings indicate that CRP promotes TSCC chemoresistance by inhibiting the activation of caspase-3/9 via the FcγRI/AKT/mTOR pathway. Thus, CRP could potentially be considered as a therapeutic target for reducing TSCC chemoresistance.

Knockdown of MALAT1 Inhibits the Progression of Chronic Periodontitis via Targeting miR-769-5p/HIF3A Axis.

PURPOSE: Chronic periodontitis (CP) is a long-lasting inflammatory disease that seriously affects oral health. This study is aimed at investigating the regulatory mechanism of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in CP. METHODS: Primary human periodontal ligament cells (PDLCs) were treated with P. gingivalis lipopolysaccharide (LPS) to establish a CP model. Quantitative real-time PCR (qRT-PCR) was used to measure the expression of MALAT1 and miR-769-5p in gingival tissues of patients with CP and LPS-treated PDLCs. Cell viability was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of inflammatory cytokines. The protein levels of caspase-3, Bax, Bcl-2, and hypoxia-inducible factor (HIF) 3A were determined by western blot assay. Dual-luciferase reporter (DLR) assay was applied to validate the target relationships between miR-769-5p and MALAT1/HIF3A. RESULTS: The expression of MALAT1 and HIF3A was enhanced, and the expression of miR-769-5p was reduced in gingival tissues of patients with CP and LPS-treated PDLCs. MALAT1 knockdown promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. MALAT1 targeted miR-769-5p and negatively regulated miR-769-5p expression. miR-769-5p overexpression promoted cell viability and inhibited inflammation and cell apoptosis in LPS-treated PDLCs. Besides, miR-769-5p targeted HIF3A and negatively modulated HIF3A expression. Both miR-769-5p inhibition and HIF3A overexpression reversed the inhibitory effects of MALAT1 silencing on LPS-induced PDLC injury in vitro. CONCLUSION: MALAT1 knockdown attenuated LPS-induced PDLC injury via regulating the miR-769-5p/HIF3A axis, which may supply a new target for CP treatment.

Silencing lncRNA HOXA10-AS decreases cell proliferation of oral cancer and HOXA10-antisense RNA can serve as a novel prognostic predictor.

OBJECTIVE: Long noncoding (lnc)RNAs regulate multiple biological processes including cancer. Oral squamous cell carcinoma (OSCC) is a common malignancy with poor prognosis. We aimed to identify the function of lncRNA HOXA10 antisense RNA (HOXA10-AS) and its clinical significance. METHODS: We used differential expression analysis to identify aberrantly expressed lncRNAs associated with OSCC. We identified key genes related to HOXA10-AS and their biological functions using bioinformatics tools and functional enrichment analyses. We predicted the function of HOXA10-AS using gene set enrichment and variation analyses and analyzed proliferation markers at the mRNA and protein levels. Finally, we silenced HOXA10-AS using antisense oligonucleotide and assessed proliferation ability using a cell counting kit (CCK8) and clone formation assays. RESULTS: In total, 506 aberrantly expressed lncRNAs were identified. HOXA10-AS was identified as a risk factor for OSCC and its expression was positively associated with tumor grade. We identified hub genes involved in regulating proliferation and predicted that HOXA10-AS is associated with an active cell cycle and increased proliferation. Silencing HOXA10-AS decreased proliferation in OSCC cell lines. CONCLUSIONS: HOXA10-AS is involved in cell proliferation and silencing it decreases proliferation. Thus, HOXA10-AS could serve as prognostic biomarker and therapeutic target for OSCC.