Guangdong Provincial Stomatological Hospital
Guangdong Provincial Stomatological Hospital
Sun L.,Sun Yat Sen University |
Liu B.,Sun Yat Sen University |
Lin Z.,Sun Yat Sen University |
Yao Y.,Sun Yat Sen University |
And 12 more authors.
Molecular Cancer | Year: 2015
Background: Salivary Adenoid cystic carcinoma (SACC) patients with local invasion and lung metastasis are often resistant to conventional therapy such as operation, chemotherapy and radiotherapy. To explore the underling mechanisms, we studied the roles of miRNA in regulating invasiveness of SACC cells. Methods: MicroRNA profiling was done in SACC cells with microarray. MiRNA mimics or antisense oligonucleotide was transfected and invasiveness of SACC cells was evaluated by adhesion assay and transwell assay. The target gene of miRNA was identified by luciferase reporter assay and "rescue" experiment. Tumor metastasis was evaluated by BALB/c-nu mice xenografts. MiRNA and its target gene expression were identified by in-situ hybridization and immunohistochemistry respectively, in 302 patients from affiliated hospitals of Sun Yat-sen University and in 148 patients from affiliated hospitals of Central South University, and correlated to the clinicopathological status of the patients. Results: MiR-320a was down-regulated in high lung metastatic ACCM and SACC-LM cells compared with the corresponding low metastatic ACC2 and SACC-83 cells, and inhibited adhesion, invasion and migration of SACC cells by targeting integrin beta 3 (ITGB3). In vivo, enforced miR-320a expression suppressed metastasis of SACC xenografts. In the two independent sets, miR-320a was downregulated in primary SACCs with metastasis compared to those without metastasis, and low expression of this miRNA predicts poor patient survival and rapid metastasis. Multivariate analysis showed that miR-320a expression was an independent indicator of lung metastasis. Conclusions: MiR-320a inhibits metastasis in SACCs by targeting ITGB3 and may serve as a therapeutic target and prognostic marker in salivary cancers. © 2015 Sun et al.; licensee BioMed Central.
Mai Z.,Sun Yat Sen University |
Peng Z.,Sun Yat Sen University |
Wu S.,Sun Yat Sen University |
Zhang J.,Guangdong Provincial Stomatological Hospital |
And 5 more authors.
PLoS ONE | Year: 2013
Fluid shear stress plays an important role in bone osteogenic differentiation. It is traditionally believed that pulsed and continuous stress load is more favorable for fracture recovery and bone homeostasis. However, according to our clinical practice, we notice that one single stress load is also sufficient to trigger osteogenic differentiation. In the present study, we subject osteoblast MC3T3-E1 cells to single bout short duration fluid shear stress by using a parallel plate flow system. The results show that 1 hour of fluid shear stress at 12 dyn/cm2 promotes terminal osteogenic differentiation, including rearrangement of F-actin stress fiber, up-regulation of osteogenic genes expression, elevation of alkaline phosphatase activity, secretion of type I collagen and osteoid nodule formation. Moreover, collaboration of BMP2 and integrin β1 pathways plays a significant role in such differentiation processes. Our findings provide further experimental evidence to support the notion that single bout short duration fluid shear stress can promote osteogenic differentiation. © 2013 Mai et al.
Mai Z.-H.,Sun Yat Sen University |
Peng Z.-L.,Sun Yat Sen University |
Zhang J.-L.,Guangdong Provincial Stomatological Hospital |
Chen L.,Sun Yat Sen University |
And 3 more authors.
Chinese Medical Journal | Year: 2013
Background Mechanical stress plays an important role in the maintenance of bone homeostasis. Current hypotheses suggest that interstitial fluid flow is an important component of the system by which tissue level strains are amplified in bone. This study aimed to test the hypothesis that the short-term and appropriate fluid shear stress (FSS) is expected to promote the terminal differentiation of pre-osteoblasts and detect the expression profile of microRNAs in the FSS-induced osteogenic differentiation in MC3T3-E1 cells. Methods MC3T3-E1 cells were subjected to 1 hour of FSS at 12 dyn/cm2 using a parallel plate flow system. After FSS treatment, cytoskeleton immunohistochemical staining and microRNAs (miRNAs) were detected immediately. Osteogenic gene expression and immunohistochemical staining for collagen type I were tested at the 24th hour after treatment, alkaline phosphatase (ALP) activity assay was performed at 24th, 48th, and 72th hours after FSS treatment, and Alizarin Red Staining was checked at day 12. Results One hour of FSS at 12 dyn/cm2 induced actin stress fiber formation and rearrangement, up-regulated osteogenic gene expression, increased ALP activity, promoted synthesis and secretion of type I collagen, enhanced nodule formation, and promoted terminal differentiation in MC3T3-E1 cells. During osteogenic differentiation, expression levels of miR-20a, -21, -19b, -34a, -34c, -140, and -200b in FSS-induced cells were significantly down-regulated. Conclusion The short-term and appropriate FSS is sufficient to promote terminal differentiation of pre-osteoblasts and a group of miRNAs may be invovled in FSS-induced pre-osteoblast differentiation.
Jiang X.,Sun Yat Sen University |
Jiang X.,Guangdong Provincial Stomatological Hospital |
Wang J.,Sun Yat Sen University |
Chen X.,Sun Yat Sen University |
And 4 more authors.
Oncotarget | Year: 2016
Chemokine (C-C motif) ligand 18 (CCL18) has been implicated in the pathogenesis and progression of various cancers; however, in oral squamous cell carcinoma (OSCC), the role of CCL18 is unknown. In this study, we found that CCL18 was overexpressed in primary OSCC tissues and was associated with an advanced clinical stage. CCL18 was found in both the cytoplasm and cell membrane of OSCC cells and was predominantly produced by cancer epithelial cells, as opposed to tumor-infiltrating macrophages. In vitro studies indicated that the effects of endogenous CCL18 on OSCC cell growth, migration, and invasion could be blocked by treatment with a neutralizing anti-CCL18 antibody or CCL18 knockdown, while exogenous recombinant CCL18 (rCCL18) rescued those effects. Akt was activated in rCCL18-treated OSCC cells, while LY294002, a pan-PI3K inhibitor, abolished both endogenous and exogenous CCL18-induced OSCC cell invasion. In vivo, LY294002 treatment attenuated rCCL18-induced OSCC cell growth. Our results indicate that CCL18 acts in an autocrine manner via Akt activation to stimulate OSCC cell growth and invasion during OSCC progression. They also provide a potential therapeutic target for the treatment of oral cancer.
PubMed | Maoming Peoples Hospital, Nanfang Hospital, Sun Yat Sen University, Guangdong Provincial Stomatological Hospital and Capital Medical University
Type: Journal Article | Journal: Journal of Cancer | Year: 2016
The development of oral squamous cell carcinoma (OSCC) is a multistep process that involves in both genetic alterations and epigenetic modifications. DJ-1, a negative regulator of tumor suppressor PTEN, functions as an oncogene in many types of cancers. However, its role in OSCC is poorly known.Immunohistochemical staining and Western blotting were performed to evaluate the expression level of DJ-1 in oral leukoplakia (OLK) and OSCC tissues respectively. Then lentiviral mediated DJ-1 shRNA was constructed and used to infect the OSCC cell lines (Tca8113 and CAL-27). MTT, cell counting, and Matrigel invasion assay were utilized to examine the effects of DJ-1 down-regulation on proliferation and invasion capacity of oral cancer cells.The immunoreactivity and expression level of DJ-1 protein was significantly increased in OLK and OSCC tissues compared with the controls. Lentiviral-delivered shRNA targeting DJ-1 could effectively knock down DJ-1 at mRNA and protein level (P<0.01). The proliferative and invasion ability of OSCC cell lines was significantly suppressed following DJ-1 inhibition (P<0.01).Our study indicated that DJ-1 is over-expressed in both oral precancer and cancer tissues and shRNA inhibition of DJ-1 expression led to decreased proliferation and invasion capability of oral cancer cells. These findings suggest that DJ-1 might be actively involved in the development of OSCC. Future studies will investigate the potential of DJ-1 as a biomarker for early detection of OSCC.
PubMed | Xaverian Brothers High School, Central South University, Sun Yat Sen University and Guangdong Provincial Stomatological Hospital
Type: | Journal: Molecular cancer | Year: 2015
Salivary Adenoid cystic carcinoma (SACC) patients with local invasion and lung metastasis are often resistant to conventional therapy such as operation, chemotherapy and radiotherapy. To explore the underling mechanisms, we studied the roles of miRNA in regulating invasiveness of SACC cells.MicroRNA profiling was done in SACC cells with microarray. MiRNA mimics or antisense oligonucleotide was transfected and invasiveness of SACC cells was evaluated by adhesion assay and transwell assay. The target gene of miRNA was identified by luciferase reporter assay and rescue experiment. Tumor metastasis was evaluated by BALB/c-nu mice xenografts. MiRNA and its target gene expression were identified by in-situ hybridization and immunohistochemistry respectively, in 302 patients from affiliated hospitals of Sun Yat-sen University and in 148 patients from affiliated hospitals of Central South University, and correlated to the clinicopathological status of the patients.MiR-320a was down-regulated in high lung metastatic ACCM and SACC-LM cells compared with the corresponding low metastatic ACC2 and SACC-83 cells, and inhibited adhesion, invasion and migration of SACC cells by targeting integrin beta 3 (ITGB3). In vivo, enforced miR-320a expression suppressed metastasis of SACC xenografts. In the two independent sets, miR-320a was downregulated in primary SACCs with metastasis compared to those without metastasis, and low expression of this miRNA predicts poor patient survival and rapid metastasis. Multivariate analysis showed that miR-320a expression was an independent indicator of lung metastasis.MiR-320a inhibits metastasis in SACCs by targeting ITGB3 and may serve as a therapeutic target and prognostic marker in salivary cancers.
Xu S.L.,Guangdong Provincial Stomatological Hospital
Zhonghua kou qiang yi xue za zhi = Zhonghua kouqiang yixue zazhi = Chinese journal of stomatology | Year: 2010
To evaluate the clinical short-term results of the acellular dermal matrix for guided bone regeneration. Sixty-four patients with bone defect in anterior maxillary area (average bone width: 3 mm) were included. Ridge-splitting technique with simultaneous placement of implants and artificial bone material implantation was performed in 21 patients (non-membrane group). Forty-three patients received the same procedure but with acellular dermal matrix covering the surgical sites (membrane group). The patients were followed up for three months and the new bone formation was checked in clinic and by X-ray. Three months after operation, the membrane group showed good osseointegration and high bone density over the implant cover screws. In the second operation, the membranes became thinner and the new bone fully covered the implant in the membrane group. The labial bone exhibited slight absorption and labial surface of 7 implants in 7 patients was exposed in non-membrane group. The width and the height of the ridge in the second operation were greater in membrane group than in non-membrane group (P < 0.05). The acellular dermal matrix can effectively resist the growth of soft tissue to allow bone regeneration around the implant.
Xue F.,University of Hong Kong |
Rabie A.B.M.,University of Hong Kong |
Luo G.,Guangdong Provincial Stomatological Hospital
Orthodontics and Craniofacial Research | Year: 2014
Structured Abstract: Objective: In this study, we performed a case-control association analysis to determine whether the candidate genes COL2A1 and IGF-1 are susceptibility genes for mandibular prognathism (MP). Methods: Eleven and five single-nucleotide polymorphisms (SNPs) located in COL2A1 and IGF-1, respectively, were selected and genotyped in 211 cases and 224 controls. The individual SNPs and the relevant haplotypes were analyzed and tested for an association with MP, to identify genes potentially associated with MP. Results: In the analysis of individual SNPs, the SNP rs1793953 in the COL2A1 gene showed a possible association with MP with regard to allelic frequency and genotypic distribution (p = 0.031; p = 0.025, respectively) in the 211 cases and 224 controls. The A allele of rs1793953 was associated with a significantly decreased risk of MP (OR: 0.74; 95% CI: 0.58-0.97). Linkage disequilibrium and haplotype analysis revealed that MP was not associated with haplotypes that included the rs1793953 alleles. IGF-1 gene did not show the association with MP. Conclusion: An association between polymorphism in the COL2A1 gene and MP was observed. The results suggested that the COL2A1 gene could be a new susceptibility gene for use in the study of genetic risk factors for MP. © 2014 John Wiley & Sons A/S.
Zhang J.,Guangdong Provincial Stomatological Hospital
Compendium of continuing education in dentistry (Jamesburg, N.J. : 1995) | Year: 2010
This study investigated the prevalence and severity of gingivitis and plaque in a representative Chinese population of adults. METHODS: Using the Loe-Silness gingivitis index (GI) and the modified Quigley-Hein plaque index (PULI), researchers examined 1143 patients from Guangzhou, Shenyang, and Nanjing for the presence of gingivitis and plaque. A two-tailed t-test was used to determine significant differences in the GI and PLI scores between gender and urban/rural areas. The data pertaining to study sites and age groups were compared using the Kruskal-Wallis one-way analysis of variances (ANOVA) by ranks. The correlation between GI/PLI and age was examined using the Pearson correlation coefficient. Age differences among three sites were analyzed with the one-way ANOVA. RESULTS: The age and urban/rural compositions (mean age 42.2 years) paralleled the 2008 China census. The overall average and standard deviation of GI and PLI were 1.101 +/- 0.239 and 3.394 +/- 0.578, respectively. Age significantly correlated with GI and PLI (P < .0001). The PLI in males was significantly higher (P < .0001) than in females; however, no significant difference was noted between GI in males compared to females. Patients in rural areas showed a significantly higher GI and PLI (t = 7.723, P < .0001; t = 7.072, P < .0001) than those in urban ones. CONCLUSIONS: Clinical trials evaluating a product's antigingivitis efficacy should recruit participants from a population that represents accurately the intended product users. Variables should include gender, race, age, and geography.
PubMed | Jinan University and Guangdong Provincial Stomatological Hospital
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2016
We previously discovered that the expression of the tumor suppressor phosphatase and tensin homolog (PTEN) was downregulated in the majority patients with tongue squamous cell carcinoma (TSCC). The aim of this study was to investigate the role of PTEN overexpression in the regulation of epithelial-mesenchymal transition (EMT) of the tongue squamous carcinoma cell line Tca8113 as well as explore the underlying mechanism. GV230 (containing the PTEN gene) and empty vectors were transfected into Tca8113 cells. After stable transfection, the messenger RNA (mRNA) and protein levels of PTEN were validated using quantitative real-time PCR (qPCR) and Western blot analysis. The growth and cell cycle were analyzed using Cell Counting Kit-8 (CCK-8) and flow cytometry, respectively. The invasion ability was measured with a transwell assay. The effects of PTEN overexpression on EMT and Hedgehog signaling were assessed by comparing Tca8113-PTEN cells with control and negative control cell groups. We found that PTEN expression was significantly upregulated after transfection. Meanwhile, upregulated PTEN inhibited the proliferation and invasion of Tca8113 cells. In addition, we observed changes in the EMT- and Hedgehog-associated proteins. These data demonstrated that PTEN upregulation could reduce invasion by inhibiting the process of EMT in Tca8113 cells, which might be related to the Hedgehog signaling pathway.