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Jiao Y.,PLA Fourth Military Medical University | Jiao Y.,Shaanxi Key Laboratory of Military Stomatology
Tumor Biology | Year: 2016

Despite advances in the roles of long non-coding RNA (lncRNA) tumor suppressor candidate 7 (TUSC7) in cancer biology, which has been identified as a tumor suppressor by regulating cell proliferation, apoptosis, migration, invasion, cell cycle, and tumor growth, the function of TUSC7 in hepatocellular carcinoma (HCC) remains unknown. In this study, we observed that the expression of TUSC7 was immensely decreased in HCC. Clinically, the lower expression of TUSC7 predicted poorer survival and may be an independent risk factor for HCC patients. Moreover, TUSC7 inhibited cell metastasis, invasion, and epithelial-to-mesenchymal transformation (EMT) through competitively binding miR-10a. Furthermore, we found that TUSC7 could decrease the expression of Eph tyrosine kinase receptor A4 (EphA4), a downstream target of miR-10a as well as an EMT suppressor, through TUSC7-miR-10a-EphA4 axis. Taken together, we demonstrate that TUSC7 suppresses EMT through the TUSC7-miR-10a-EphA4 axis, which may be a potential target for therapeutic intervention in HCC. © 2016 The Author(s) Source


Jiao Y.,PLA Fourth Military Medical University | Jiao Y.,Shaanxi Key Laboratory of Military Stomatology | Ma S.,PLA Fourth Military Medical University | Ma S.,Shaanxi Key Laboratory of Military Stomatology | And 18 more authors.
PLoS ONE | Year: 2016

Purpose To investigate the involvement of intrinsic mitochondrial apoptosis in dental monomerinduced cytotoxicity and the influences of N-Acetyl cysteine (NAC) on this process. Methods Human dental pulp cells (hDPCs) were exposed to several dental monomers in the absence or presence of NAC, and cell viability, intracellular redox balance, morphology and function of mitochondria and key indicators of intrinsic mitochondrial apoptosis were evaluated using various commercial kits. Results Dental monomers exerted dose-dependent cytotoxic effects on hDPCs. Concomitant to the over-production of reactive oxygen species (ROS) and depletion of glutathione (GSH), differential changes in activities of superoxide dismutase, glutathione peroxidase, and catalase were detected. Apoptosis, as indicated by positive Annexin V/propidium iodide (PI) staining and activation of caspase-3, was observed after dental monomer treatment. Dental monomers impaired the morphology and function of mitochondria, and induced intrinsic mitochondrial apoptosis in hDPCs via up-regulation of p53, Bax and cleaved caspase-3, and down-regulation of Bcl-2. NAC restored cell viability, relieved oxidative stress and blocked the apoptotic effects of dental monomers. Conclusions Dental monomers induced oxidative stress and mitochondrial intrinsic apoptosis in hDPCs. NAC could reduce the oxidative stress and thus protect hDPCs against dental monomerinduced apoptosis. © 2016 Jiao et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in anymedium, provided the original author and source are credited. Source


Jiao Y.,PLA Fourth Military Medical University | Jiao Y.,Shaanxi Key Laboratory of Military Stomatology | Ma S.,PLA Fourth Military Medical University | Ma S.,Shaanxi Key Laboratory of Military Stomatology | And 6 more authors.
Medical Science Monitor | Year: 2015

Resin monomers from dental composite materials leached due to incomplete polymerization or biodegradation may cause contact allergies and damage dental pulp. The cytotoxicity of dental resin monomers is due to a disturbance of intracellular redox equilibrium, characterized by an overproduction of reactive oxygen species (ROS) and depletion of reduced glutathione (GSH). Oxidative stress caused by dental resin monomers leads to the disturbance of vital cell functions and induction of cell apoptosis in affected cells. The nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway plays a key role in the cellular defense system against oxidative and electrophilic stress. Epigallocatechin-3-gallate (EGCG) can activate the Nrf2 pathway and induce expression of a multitude of antioxidants and phase II enzymes that can restore redox homeostasis. Therefore, here, we tested the hypothesis that EGCG-mediated protection against resin monomer cytotoxicity is mediated by activation of the Nrf2 pathway. This study will help to elucidate the mechanism of resin monomer cytotoxicity and provide information that will be helpful in improving the biocompatibility of dental resin materials. © Med Sci Monit. Source


Liu Q.,PLA Fourth Military Medical University | Jiao Y.,PLA Fourth Military Medical University | Jiao Y.,Shaanxi Key Laboratory of Military Stomatology | Zhao Y.,College of Logistics | And 10 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2016

Oral cancer is one of the ten most common cancers in the world. The objective of this meta-analysis was to determine the association between tea consumption and risk of oral cancer. A comprehensive literature search was performed in PubMed, Embase and reference lists. A meta-analysis was performed by STATA software. Fifteen studies involving 5,491 oral cancer cases examining the association between tea consumption and risk of oral cancer were included. Among all the studies, 12 studies were case-control, and 3 were cohort studies. The relative risks (RRs) were pooled using a random-effects model. Relative risks with 95% confidence intervals (CIs) were used in the analyses. The pooled RR of included studies between tea drinking and risk of oral cancer was 0.85 (95% CI: 0.75-0.93). After stratifying by the study designs, a significant inverse association between tea drinking and oral cancer risk was observed in both cohort studies (n = 3; RR = 0.81; 95% CI: 0.66-1.0) and the case-control studies (n = 12; RR = 0.858; 95% CI: 0.777-0.948). A significant evidence of dose-response relationship was detected between tea consumption and oral cancer risk (P < 0.001). Findings from this meta-analysis suggest that tea consumption may reduce the risk of oral cancer. Because of the limited number of studies, further high-quality cohort or case-control studies are needed studies are needed to explore the protective effect of tea on oral cancer. © 2016, International Journal of Clinical and Experimental Medicine. All rights reserved. Source

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