Electrophoretic deposition of magnesium oxide coating on micro-arc oxidized titanium for antibacterial activity and biocompatibility.

Titanium (Ti) dental implants face risks of early failure due to bacterial adhesion and biofilm formation. It is thus necessary to endow the implant surface with antibacterial ability. In this study, magnesium oxide (MgO) coatings were prepared on Ti by combining micro-arc oxidation (MAO) and electrophoretic deposition (EPD). The MgO nanoparticles homogeneously deposited on the microporous surface of MAO-treated Ti, yielding increasing coverage with the EPD time increased to 15 to 60 s. After co-culture with Porphyromonas gingivalis (P. gingivalis) for 24 h, 48 h, and 72 h, the coatings produced antibacterial rates of 4-53 %, 27-71 %, and 39-79 %, respectively, in a dose-dependent manner. Overall, EPD for 45 s offered satisfactory comprehensive performance, with an antibacterial rate 79 % at 72 h and a relative cell viability 85 % at 5 d. Electron and fluorescence microscopies revealed that, both the density of adherent bacterial adhesion on the surface and the proportion of viable bacteria decreased with the EPD time. The morphology of cells on the surface of each group was intact and there was no significant difference among the groups. These results show that, the MgO coating deposited on MAO-treated Ti by EPD had reasonably good in vitro antibacterial properties and cytocompatibility.

Lycorine upregulates the expression of RMB10, promotes apoptosis and inhibits the proliferation and migration of cervical cancer cells.

Although there are numerous treatment strategies, including surgery and chemotherapy, the prognosis of cervical cancer remains far from satisfactory. There is an urgent need to develop more effective, more tolerable and safer therapeutics for the treatment of cervical cancer. Lycorine is a natural plantextract that has been previously found to confer anti­tumor activities. Therefore, in the present study, the effects of lycorine and its possible mechanism of action in cervical cancer were investigated. Cell Counting Kit­8, wound healing and Transwell assays were used to verify the proliferation and migration of HeLa cells following lycorine intervention. The results demonstrated that lycorine significantly inhibited the proliferation and migration of HeLa cells. RNA binding motif 10 (RBM10) is a protein associated with apoptosis. It has been suggested that lycorine can affect the expression of RBM10. Flow cytometry demonstrated that lycorine may inhibit the initiation and progression of cervical cancer by promoting apoptosis, which may be mediated through the upregulation of RBM10 expression and increasing TNF­α levels. Xenograft mouse experiments indicated that when lycorine was injected through the tail vein, HeLa tumor growth was inhibited. Mechanistically, western blotting demonstrated that lycorine significantly inhibited the activation of the Akt signaling pathway and potentially reversed epithelial­mesenchymal transition, which was also mediated by RBM10. Furthermore, following RBM10 knockdown with small interfering­RNA, the inhibitory effects of lycorine on cervical cancer was significantly abrogated. Overall, results of the present study suggest that lycorine can upregulate the expression of RBM10 and inhibit the proliferation and migration of cervical cancer cells.

Adipose-derived stem cells postpone the progression of Sjögren's syndrome by upregulating the Hippo signaling pathway.

The aim of the present study was to explore the effect and mechanism of action of adipose-derived stem cells (ADSCs) on Sjögren syndrome (SS) to develop novel and more effective methods for SS treatment. ADSCs, dexamethasone or normal saline was injected into the submandibular gland (SMG) of three 12-week-old non-obese diabetic (NOD) mice. The degree of lymphocyte infiltration was considered as a criterion for judging disease progression, hematoxylin and eosin staining was performed to observe the pathological state, and the expression levels of TAZ, E-cadherin and α-catenin were assessed by western blotting. ADSC transplantation triggered an inhibitory effect on the progression of SS, which was slightly stronger compared with that of dexamethasone treatment. This was found to be related to the Hippo signaling pathway. In addition, TAZ protein expression levels decreased gradually with the progression of the disease; immunofluorescence staining showed that the expression of E-cadherin and TAZ followed similar trends. Notably, the expression of TAZ, p-TAZ, E-cadherin and α-catenin in NOD mice were lower compared with that in Control mice. Similarly, the ratio of p-TAZ/TAZ also decreased, which means that the activation level of Hippo signal pathway decreased. The results suggest that ADSCs may exert a therapeutic effect against SS and may postpone its progression by upregulating the Hippo signaling pathway.

Adipose-derived stem cells promote the proliferation, migration, and invasion of oral squamous cell carcinoma cells by activating the Wnt/planar cell polarity signaling pathway.

Background: Oral squamous cell carcinoma (OSCC) is the most common malignancy of the oral and maxillofacial region. Adipose-derived stem cells (ADSCs) interact with a variety of malignant tumors to promote their proliferation and metastasis. Abnormalities in Wnt/planar cell polarity (PCP) signaling and overactivation of the signaling pathway are considered to be related to the occurrence and development of various malignant tumors. In order to determine whether ADSC can promote tumorigenesis in OSCC and its molecular mechanism, we conducted a series of studies. Methods: The effect of ADSCs on the occurrence and development of OSCC was studied in vivo and in vitro, and the molecular mechanism was investigated using Western blot and immunofluorescence (IHC) assays. Results: The results revealed that ADSCs could promote the proliferation, invasion, and migration of OSCC cells in a dose- and time-dependent manner. With regard to the mechanism, the expression of collagen triple helix repeat-containing protein 1 (CTHRC1) and phospho-c-Jun (p-c-Jun) increased significantly with enhancement of the interaction between ADSCs and OSCC cells, indicating that the Wnt/PCP signaling pathway was overactivated. Conclusions: ADSCs promote the pathogenesis of OSCC by activating the Wnt/PCP signaling pathway, suggesting that proteins related to this pathway may be potential therapeutic targets for OSCC.

CTHRC1 overexpression promotes cervical carcinoma progression by activating the Wnt/PCP signaling pathway.

The tumorigenesis and metastasis of tumors are associated with human collagen triple helix repeats containing 1 (CTHRC1). To study the effects and possible impacting mechanisms of CTHRC1 on human cervical carcinoma development, samples of paraffin­embedded cervical carcinoma and HeLa cells were examined. Immunofluorescence, cell wound scratch assay, western blot analysis and Transwell invasion assay were used to evaluate HeLa cells in response to silencing of the CTHRC1 gene in cervical carcinoma. The expression levels of gap­associated proteins of the Wnt/PCP pathway in paraffin­embedded cervical carcinoma samples were also evaluated by immunohistochemical staining. CTHRC1 promoted the migration and invasion of HeLa cells in vitro, downregulated Ror2 and p­c­Jun and activated the Wnt/PCP pathway. Furthermore, the expression of p­c­Jun, Ror2 and Wnt5a was increased after overexpression of CTHRC1 as revealed in HeLa cells compared to control group. The present experiments revealed that CTHRC1 promoted HeLa cell progression by activating the Wnt/PCP signaling pathway and may play a key role in the invasion and metastasis of cervical carcinoma.

HOTAIRM1 competed endogenously with miR-148a to regulate DLGAP1 in head and neck tumor cells.

This study is aimed to explore the regulatory effect of lncRNA HOTAIR/miR-148a/DLGAP1 axis on head and neck tumor (HNT) cell growth, cell mobility, and invasiveness. HOTAIRM1, miR-148a, and DLGAP1 level in HNT tissues and adjacent normal tissues were measured by qRT-PCR. Cell Counting Kit-8 (CCK-8) and Transwell (migration and invasion) assay were used to survey the influence of HOTAIRM1, miR-148a, and DLGAP1 on Fadu cells. Nude mouse xenograft was utilized to validate the influence of HOTAIRM1 in vivo. Dual-luciferase reporter assay confirms the relationship between HOTAIRM1 and miR-148a, miR-148a, and DLGAP1. The expression level of HOTAIRM1 was downregulated in human HNT tissues and cells. Overexpression of HOTAIRM1 significantly moderated Fadu cells proliferation, apoptosis, migration, and invasion in vitro and impaired the tumorigenesis in vivo. The expression level of miR-148a was upregulated in human HNT tissue compared to the adjacent tissues. We identified that miR-148a was a target of HOTAIRM1 and its expression levels were reduced by HOTAIRM1. Transfection of miR-148a mimics increased proliferation, migration, and invasion of Fadu cells. DLGAP1 was identified as a novel target of miR-148a and its expression level was promoted by either HOTAIRM1 overexpression or miR-148a knockdown. Overexpression of DLGAP1 also facilitated the cell viability and metastasis of Fadu cells. HOTAIRM1 was confirmed as a tumor suppressor via sponging miR-148a and promote the expression of DLGAP1, which could be regarded as an important target for the prevention and treatment of HNT.

Nicotine may promote tongue squamous cell carcinoma progression by activating the Wnt/ß-catenin and Wnt/PCP signaling pathways.

To investigate the effects and the possible underlying mechanisms of nicotine stimulation on tongue squamous cell carcinoma (TSCC) progression, a TSCC cell line Cal27 and 34 samples of paraffin-embedded TSCC were examined. Immunofluorescence, western blot analysis, and TOP/FOP flash, CCK-8, wound healing and Transwell invasion assays were used to evaluate Cal27 in response to nicotine stimulation. We also investigated expression levels of related proteins of Wnt/ß-catenin and Wnt/PCP pathways in paraffin-embedded TSCC samples with or without a history of smoking by immunohistochemistry. Nicotine stimulation can promote proliferation, migration, and invasion of TSCC cells in vitro, downregulate E-cadherin, and activate the Wnt/ß-catenin and Wnt/PCP pathways, which could be antagonized by the α7 nicotine acetylcholine receptor (α7 nAChR) inhibitor α-BTX. Moreover, the expression levels of ß-catenin, Wnt5a and Ror2 were higher in TSCC patients with a history of smoking than those without a history of smoking. Our results suggest nicotine may promote tongue squamous carcinoma cells progression by activating the Wnt/ß-catenin and Wnt/PCP signaling pathways and may play a significant role in the progression and metastasis of smoking-related TSCC.

Effects of alveolar ridge preservation on delayed implant osseointegration.

To evaluate the effects of alveolar ridge preservation with Bio-Oss bone substitute (Geistlich Pharma) on delayed implant osseointegration. The 3rd and 4th left and right mandibular premolars were extracted from four adult healthy male and female dogs. For the experimental group, we randomly selected two extraction sockets in each dog to be filled with Bio-Oss bone substitute (Geistlich Pharma). The two remaining extraction sockets remained untreated and served as the control group. Three months after Bio-Oss placement, dental implants were inserted into the alveolar bone of the experimental group and the control group. The osteogenic activity of the bone around the implants was assessed by evaluating the histological morphology and by estimating histomorphometric parameters at 3 and 6 months after delayed implantation. At 3 months, Goldner's trichrome staining analysis showed that the bone-implant contact rate and mineralised bone area around the implant were significantly higher in the experimental group (75.98% ± 8.97% and 69.52% ± 9.63%, respectively) than in the control group (56.13% ± 8.18% and 52.82% ± 7.25%, respectively; P < 0.05). However, at 6 months, the two groups showed no significant difference. Fluorescence microscopy analysis revealed that the average mineralisation apposition rate of the bone tissue around the dental implant in the experimental group at 3 and 6 months was 6.80 ± 0.43 µm and 8.38 ± 0.84 µm, respectively, which was significantly higher than the rate in the control group (P < 0.05). These data indicated that alveolar ridge preservation by using Bio-Oss placement can promote osseointegration of delayed implantation. This may be a promising option for clinical use.

N-glycosylation induces the CTHRC1 protein and drives oral cancer cell migration.

Oral squamous cell carcinoma (OSCC) is one of the most pernicious malignancies, but the mechanisms underlying its development and progression are poorly understood. One of the key pathways implicated in OSCC is the canonical Wnt/ß-catenin signaling pathway. Previously, we reported that canonical Wnt signaling functions in a positive feedback loop with the DPAGT1 gene, a principal regulator of the metabolic pathway of protein N-glycosylation, to hyperglycosylate E-cadherin and reduce intercellular adhesion. Here, we show that in OSCC, DPAGT1 and canonical Wnt signaling converge to up-regulate CTHRC1 (collagen triple helix repeat containing 1), an N-glycoprotein implicated in tumor invasion and metastasis. We found that in human OSCC specimens, amplification of the levels of CTHRC1 was associated with its hyperglycosylation. Partial inhibition of DPAGT1 expression in OSCC CAL27 cells reduced CTHRC1 abundance by increasing protein turnover, indicating that N-glycosylation stabilizes CTHRC1. Additionally, canonical Wnt signaling promoted ß-catenin/T-cell factor transcriptional activity at the CTHRC1 promoter to further elevate CTHRC1 levels. We demonstrate that DPAGT1 promotes cell migration and drives the localization of CTHRC1 to cells at the leading edge of a wound front coincident with drastic changes in cell morphology. We propose that in OSCC, dysregulation of canonical Wnt signaling and DPAGT1-dependent N-glycosylation induces CTHRC1, thereby driving OSCC cell migration and tumor spread.

[Clinical retrospective study on membrane guided bone tissue regeneration technique in dental implants in the anterior maxilla].

PURPOSE: The purpose of this study was to investigate the effect of Bio-Gide in MGBR (membrane guided bone regeneration ) in the anterior maxilla dental implant therapy. METHODS: Fifty five cases underwent dental implant therapy in the anterior maxilla with insufficient maxillary anterior bone, including 29 patients with embedded 40 implants using MGBR and 26 patients with embedded 40 implants without using MGBR. The condition of bone around implant before implantation and before final restoration was observed and recorded. The thickness of the bone was measured with vernier caliper, the density and the bone loss were determined by X-ray examination. The results were analyzed with X-ray radiographs image analysis system (Sidexis) and SPSS16.0 software package. RESULTS: Univariate analysis showed that there was significant difference in the thickness and the density of the bone between before implant operation and before restoration(P<0.05). There was significant difference between the thickness and the density of the bone between with and without MGBR(P<0.05). CONCLUSIONS: These results suggest that the thickness and the density of the bone in the group with MGBR is better than the group without MGBR. It is recommended to use MGBR in dental implant therapy in the anterior maxilla with insufficient bone.