Shen Z.,Guangdong Medical College |
Jiang X.,Guangdong Medical College |
Zeng C.,Guangdong Medical College |
Zheng S.,Hainan Medical College |
And 7 more authors.
BMC Cancer | Year: 2013
Background: Overexpression of ubiquitin-conjugating enzyme 2C (UBE2C) has been detected in many types of human cancers, and is correlated with tumor malignancy. However, the role of UBE2C in human nasopharyngeal carcinoma (NPC) is unclear. In this study, we investigated the role of aberrant UBE2C expression in the progression of human NPC.Methods: Immunohistochemical analysis was performed to detect UBE2C protein in clinical samples of NPC and benign nasopharyngeal tissues, and the association of UBE2C expression with patient clinicopathological characteristics was analyzed. UBEC2 expression profiles were evaluated in cell lines representing varying differentiated stages of NPC and immortalized nasopharyngeal epithelia NP-69 cells using quantitative RT-PCR, western blotting and fluorescent staining. Furthermore, UBE2C was knocked down using RNA interference in these cell lines and proliferation and cell cycle distribution was investigated.Results: Immunohistochemical analysis revealed that UBE2C protein expression levels were higher in NPC tissues than in benign nasopharyngeal tissues (P<0.001). Moreover, high UBE2C protein expression was positively correlated with tumor size (P=0.017), lymph node metastasis (P=0.016) and distant metastasis (P=0.015) in NPC patients. In vitro experiments demonstrated that UBE2C expression levels were inversely correlated with the degree of differentiation of NPC cell lines, whereas UBE2C displayed low level of expression in NP-69 cells. Knockdown of UBE2C led to significant arrest at the S and G2/M phases of the cell cycle, and decreased cell proliferation was observed in poorly-differentiated CNE2Z NPC cells and undifferentiated C666-1 cells, but not in well-differentiated CNE1 and immortalized NP-69 cells.Conclusions: Our findings suggest that high expression of UBE2C in human NPC is closely related to tumor malignancy, and may be a potential marker for NPC progression. © 2013 Shen et al.; licensee BioMed Central Ltd.
Liu Z.,Southern Medical University |
Li X.,Southern Medical University |
He X.,Peoples Hospital of Zhongshan City |
Jiang Q.,Southern Medical University |
And 6 more authors.
International Journal of Cancer | Year: 2011
Human NESG1 (CCDC19) gene was originally isolated in our laboratory from human nasopharynx tissue. However, the biological and clinical significances of this gene remain largely unknown. In this report, two errors in the originally submitted sequence of human NESG1 gene were found, and the open reading frame sequence of NESG1 (Accession number: NM-012337.1) was revised and updated in the NCBI database (Accession number: NM-012337.2). The antibody raised against the revised sequence of NESG1 detected a single band of 66 kD in human nasopharynx tissues. NESG1 transcripts were specifically expressed in the nasopharynx epithelium. Expression of NESG1 transcripts and protein was downregulated or absent in nasopharyngeal carcinoma (NPC) tissues and cell lines in comparison to that in the normal nasopharynx tissues. The levels of NESG1 protein were significantly greater in the low-grade NPC tissues than that in the high-grade NPC tissues. Induced expression of NESG1 in otherwise NESG1-negative 5-8F cells not only significantly decreased cell proliferation, G1-S phase transition, but also markedly inhibited the ability of cell migration and invasion as well as in vivo tumorigenesis. Furthermore, NESG1 also significantly regulated the expression of cell cycle regulator CCNA1 and p21. Our findings first provided evidence that NESG1 may act as a tumor suppressor by inhibiting cell proliferation, invasion and migration of NPC cells. © 2010 UICC.
Si J.-G.,Peoples Hospital of Zhongshan City |
Su Y.-Y.,Peoples Hospital of Zhongshan City |
Han Y.-H.,Peoples Hospital of Zhongshan City |
Chen R.-H.,Peoples Hospital of Zhongshan City
Genetic Testing and Molecular Biomarkers | Year: 2014
Objective: The aim of the current meta-analysis was to comprehensively assess the role of RASSF1A promoter methylation in the pathogenesis of ovarian cancer. Method: A range of electronic databases were searched: Web of Science (1945-2013), the Cochrane Library Database (Issue 12, 2013), PubMed (1966-2013), EMBASE (1980-2013), CINAHL (1982-2013), and the Chinese Biomedical Database (1982-2013) without language restrictions. Meta-analysis was conducted using the STATA 12.0 software. The crude odds ratio (OR) with its corresponding 95% confidence interval (CI) was calculated. Results: Twelve clinical cohort studies with a total of 739 ovarian cancer patients were included in the current meta-analysis. The results of our meta-analysis suggested that the frequency of RASSF1A promoter methylation in cancer tissues was higher compared with benign, adjacent, and normal tissues (cancer tissues vs. benign tissues: OR=9.92, 95% CI: 7.67-12.82, p<0.001; cancer tissues vs. adjacent tissues: OR=68.15, 95% CI: 39.30-118.18, p<0.001; cancer tissues vs. normal tissues: OR=30.71, 95% CI: 23.12-40.80, p<0.001; respectively). Subgroup analysis based on ethnicity and sample types revealed that RASSF1A gene methylation was closely associated with the pathogenesis of ovarian cancer in all subgroups (all p<0.05). Conclusion: Our findings indicated that abnormal RASSF1A promoter methylation may be strongly correlated with the pathogenesis of ovarian cancer. © Mary Ann Liebert, Inc. 2014.
Kock J.,University Hospital Freiburg |
Rosler C.,University Hospital Freiburg |
Zhang J.,University Hospital Freiburg |
Zhang J.,Peoples Hospital of Zhongshan City |
And 3 more authors.
PLoS ONE | Year: 2012
Experimental studies on hepatitis B virus (HBV) replication are commonly done with human hepatoma cells to reflect the natural species and tissue tropism of the virus. However, HBV can also replicate, upon transfection of virus coding plasmids, in cells of other species. In such cross-species transfection experiments with chicken LMH hepatoma cells, we previously observed the formation of HBV genomes with aberrant electrophoretic mobility, in addition to the those DNA species commonly seen in human HepG2 hepatoma cells. Here, we report that these aberrant DNA forms are mainly due to excessive splicing of HBV pregenomic RNA and the abundant synthesis of spliced DNA products, equivalent to those also made in human cells, yet at much lower level. Mutation of the common splice acceptor site abolished splicing and in turn enhanced production of DNA from full-length pgRNA in transfected LMH cells. The absence of splicing made other DNA molecules visible, that were shortened due to the lack of sequences in the core protein coding region. Furthermore, there was nearly full-length DNA in the cytoplasm of LMH cells that was not protected in viral capsids. Remarkably, we have previously observed similar shortened genomes and non-protected viral DNA in human HepG2 cells, yet exclusively in the nucleus where uncoating and final release of viral genomes occurs. Hence, two effects reflecting capsid disassembly in the nucleus in human HepG2 cells are seen in the cytoplasm of chicken LMH cells. © 2012 Köck et al.
Shan P.-F.,Zhejiang University |
Shan P.-F.,Central South University |
Lu Y.,Peoples Hospital of Zhongshan City |
Lu Y.,Central South University |
And 4 more authors.
PLoS ONE | Year: 2011
Vascular calcification, which results from a process osteoblastic differentiation of vascular smooth muscle cells (VSMCs), is a major risk factor for cardiovascular morbidity and mortality. Apelin is a recently discovered peptide that is the endogenous ligand for the orphan G-protein-coupled receptor, APJ. Several studies have identified the protective effects of apelin on the cardiovascular system. However, the effects and mechanisms of apelin on the osteoblastic differentiation of VSMCs have not been elucidated. Using a culture of calcifying vascular smooth muscle cells (CVMSCs) as a model for the study of vascular calcification, the relationship between apelin and the osteoblastic differentiation of VSMCs and the signal pathway involved were investigated. Alkaline phosphatase (ALP) activity and osteocalcin secretion were examined in CVSMCs. The involved signal pathway was studied using the extracellular signal-regulated kinase (ERK) inhibitor, PD98059, the phosphatidylinositol 3-kinase (PI3-K) inhibitor, LY294002, and APJ siRNA. The results showed that apelin inhibited ALP activity, osteocalcin secretion, and the formation of mineralized nodules. APJ protein was detected in CVSMCs, and apelin activated ERK and AKT (a downstream effector of PI3-K). Suppression of APJ with siRNA abolished the apelin-induced activation of ERK and Akt. Furthermore, inhibition of APJ expression, and the activation of ERK or PI3-K, reversed the effects of apelin on ALP activity. These results showed that apelin inhibited the osteoblastic differentiation of CVSMCs through the APJ/ERK and APJ/PI3-K/AKT signaling pathway. Apelin appears to play a protective role against arterial calcification. © 2011 Shan et al.
Lu Y.,Peoples Hospital of Zhongshan City |
Zhu X.,Central South University |
Liang G.-X.,Peoples Hospital of Zhongshan City |
Cui R.-R.,Central South University |
And 11 more authors.
Amino Acids | Year: 2012
Apelin receptor (APJ) deficiency has been reported to be preventive against atherosclerosis. However, the mechanism of this effect remains unknown. In this study, quantitative real-time RT-PCR, Western blotting and ELISA analyses revealed a significant increase in the expression of intercellular adhesion molecule-1(ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and monocyte chemoattractant protein-1 (MCP-1) in human umbilical vein endothelial cells (HUVECs) treated with apelin. Inhibitors of cellular signal transduction molecules were used to demonstrate involvement of nuclear factor kappa-B (NF-κB) and c-Jun N-terminal kinase (JNK) pathways in apelin-APJ-induced activation of adhesion molecules and chemokines. Inhibition of APJ expression by RNA interference abrogated apelin-induced expression of adhesion molecules and chemokines and apelin-stimulated cellular signal transduction in HUVECs. The apelin-APJ system in endothelial cells is involved in the expression of adhesion molecules and chemokines, which are important for the initiation of endothelial inflammation-related atherosclerosis. Therefore, apelin-APJ and the cell signaling pathways activated by this system in endothelial cells may represent targets for therapy of atherosclerosis. © 2012 Springer-Verlag.
Tu L.,Southern Medical University |
Liu Z.,Southern Medical University |
He X.,Peoples hospital of Zhongshan City |
He Y.,Nanchang University |
And 7 more authors.
Molecular Cancer | Year: 2010
Background: The aim of the present study was to analyze the expression of eukaryotic translation initiation factor 4 gamma 1 (EIF4G1) in nasopharyngeal carcinoma (NPC) and its correlation with clinicopathologic features, including patients' survival time.Methods: Using real-time PCR, we detected the expression of EIF4G1 in normal nasopharyngeal tissues, immortalized nasopharyngeal epithelial cell lines NP69, NPC tissues and cell lines. EIF4G1 protein expression in NPC tissues was examined using immunohistochemistry. Survival analysis was performed using Kaplan-Meier method. The effect of EIF4G1 on cell invasion and tumorigenesis were investigated.Results: The expression levels of EIF4G1 mRNA were significantly greater in NPC tissues and cell lines than those in the normal nasopharyngeal tissues and NP69 cells (P < 0.001). Immunohistochemical analysis revealed that the expression of EIF4G1 protein was higher in NPC tissues than that in the nasopharyngeal tissues (P < 0.001). In addition, the levels of EIF4G1 protein in tumors were positively correlated with tumor T classification (P = 0.039), lymph node involvement (N classification, P = 0.008), and the clinical stages (P = 0.003) of NPC patients. Patients with higher EIF4G1 expression had shorter overall survival time (P = 0.019). Multivariate analysis showed that EIF4G1 expression was an independent prognostic indicator for the overall survival of NPC patients. Using shRNA to knock down the expression of EIF4G1 not only markedly inhibited cell cycle progression, proliferation, migration, invasion, and colony formation, but also dramatically suppressed in vivo xenograft tumor growth.Conclusion: Our data suggest that EIF4G1 can serve as a biomarker for the prognosis of NPC patients. © 2010 Tu et al; licensee BioMed Central Ltd.
PubMed | Weifang Medical University, Peoples Hospital of Zhongshan City and Sun Yat Sen University
Type: Comparative Study | Journal: BMC neurology | Year: 2016
The underlying causes of minor stroke are difficult to assess. Here, we evaluate the reliability of the Chinese Ischemic Stroke Subclassification (CISS) system in patients with minor stroke, and compare it to the Trial of Org 10172 in Acute Stroke Treatment (TOAST) system.A total of 320 patients with minor stroke were retrospectively registered and categorized into different subgroups of the CISS and TOAST by two neurologists. Inter- and intra-rater agreement with the two systems were assessed with kappa statistics.The percentage of undetermined etiology (UE) cases in the CISS system was 77.3% less than that in the TOAST system, which was statistically significant (P<0.001). The percentage of large artery atherosclerosis (LAA) in the CISS system was 79.7% more than that in the TOAST system, which was also statistically significant (P<0.001). The kappa values for inter-examiner agreement were 0.898 (P=0.031) and 0.732 (P=0.022) for the CISS and TOAST systems, respectively. The intra-observer reliability indexes were moderate (0.569 for neurologist A, and 0.487 for neurologist B).The CISS and TOAST systems are both reliable in classifying patients with minor stroke. CISS classified more patients into known etiologic categories without sacrificing reliability.
PubMed | Peoples Hospital of Zhongshan City, Wu Jing Zong Dui Hospital of Guangdong Province, Southern Medical University and Shantou University
Type: Journal Article | Journal: PloS one | Year: 2014
Type 2 diabetes is often accompanied by altered cardiometabolic risk profiles, including abdominal obesity, hypertension, and dyslipidaemia. The association of altered cardiometabolic risk profiles with chronic complications of diabetes is not well investigated.We recruited 2954 type 2 diabetes patients with a body mass index 25 kg/m2 who visited the diabetes clinics of 62 hospitals in 21 cities in Guangdong province of China from August 2011 to March 2012. Demographic characteristics, personal and family medical histories, and data on chronic complications of diabetes were collected. Clinical examinations and laboratory assessment were conducted.Abdominal obesity was found in 91.6% of the study population, elevated blood pressure in 78.3%; elevated serum triacylglycerols in 57.8%, and reduced serum HDL-C in 55.9%. Among the cardiometabolic risk factors, elevated blood pressure was significantly associated with almost all the chronic complications of diabetes. After adjusting for age, gender, duration of diabetes, and HbA1c, elevated blood pressure was significantly associated with diabetic retinopathy (OR 1.63, 95% CI: 1.22-2.19), diabetic nephropathy (OR 3.16, 95% CI: 2.25-4.46), cardiovascular disease (OR 2.71, 95% CI: 1.70-4.32), and stroke (OR 1.90, 95% CI: 1.15-3.12). Abdominal adiposity was significantly associated with diabetic nephropathy (OR 1.39, 95% CI: 1.11-1.74). Elevated triacylglycerols was significantly associated with diabetic retinopathy (OR 1.29, 95% CI: 1.05-1.58) and diabetic nephropathy (OR 1.30, 95% CI: 1.05-1.58). Reduced HDL-C was significantly associated with stroke (OR 1.41, 95% CI: 1.05-1.88).Altered cardiometabolic risk profiles, and elevated blood pressure in particular, were significantly associated with chronic complications in overweight and obese patients with type 2 diabetes. Future studies on the prevention of chronic complications of diabetes might make lowering blood pressure a primary target.
PubMed | Peoples Hospital of Zhongshan City
Type: Comparative Study | Journal: International nursing review | Year: 2013
The concept of caring is important to both patients and nurses. If patients and nurses perceive caring behaviours differently, patients may not have their needs met or will be dissatisfied with the nursing.This study conducted in mainland China compared the perceptions of nurses and patients concerning nurses caring behaviours.From November 2011 to June 2012, 680 patients and 540 of their nurses in five hospitals in southern, central and eastern China were invited to complete a descriptive comparative survey with four subcategories, the Caring Behaviors Inventory-24. Respondents scored each of the 24 items on the survey from 1 (low) to 6 (high). Of those invited, 595 patients (87.50%) and 445 (82.41%) nurses completed the survey.The mean item score on the Caring Behaviors Inventory-24 was 4.32 and 4.96 for patients and nurses, respectively. The subcategory with the highest mean score for both groups was knowledge and skills (4.73, 5.25), and the lowest for both groups was positive connectedness (3.98, 4.51). Nurses scores were significantly higher than those of patients for all four subcategories (P < 0.001).The gap between the two groups indicates that nurses need to improve their understanding and response to patients actual and perceived needs and expectations. In China, patients require more support from nurses of their psychological needs.Participants came from a limited number of hospitals in three cities. A larger sample from different hospitals in mainland China could have increased the power of the study.