Key Laboratory for Medical Molecular Diagnostics of Guangdong Province

Dongguan, China

Key Laboratory for Medical Molecular Diagnostics of Guangdong Province

Dongguan, China
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Huang G.-L.,Guangdong Medical College | Huang G.-L.,Key Laboratory for Medical Molecular Diagnostics of Guangdong Province | Qiu J.-H.,Huizhou First Hospital | Li B.-B.,Guangdong Medical College | And 9 more authors.
Pathology and Oncology Research | Year: 2013

Pin1 (peptidylprolyl cis/trans isomerase, NIMA-interacting 1) plays a key role in a number of diseases including cancer and Alzheimer disease. Previous studies have identified a wide range of phosphoproteins as Pin1 substrates. Related pathways were analyzed separately. The aim of this study was to provide a comprehensive picture involving Pin1 regulation. A genome-wide mRNA expression microarray was carried out using the RNA isolation from Pin1 +/+ and Pin1 -/- mouse embryonic fibroblast (MEF) cells. Signaling pathways regulated by Pin1 were analyzed with the utility of KEGG pathway and GO annotation. An expression pattern regulated by Pin1 was revealed. A total of 606 genes, 375 being up-regulated and 231 down-regulated, were differentially expressed when comparing Pin1 +/+ to Pin1 -/- MEF cells. Totally 48 pathways were shown to be regulated by Pin1 expression in KEGG pathway analysis. In the GO annotation system, 19 processes on biological processes, 15 processes on cellular components, and 18 processes on molecular functions were found to be in the regulation of Pin1 expression. Pathways related to immune system and cancer showed most significant association with Pin1 regulation. Pin1 is an important regulator in a wide range of signaling pathways that were related to immune system and cancer. © 2013 Arányi Lajos Foundation.


Delaney J.R.,University of Washington | Sutphin G.L.,University of Washington | Dulken B.,University of Washington | Sim S.,University of Washington | And 40 more authors.
Aging Cell | Year: 2011

Activation of Sir2 orthologs is proposed to increase lifespan downstream of dietary restriction. Here, we describe an examination of the effect of 32 different lifespan-extending mutations and four methods of DR on replicative lifespan (RLS) in the short-lived sir2Δ yeast strain. In every case, deletion of SIR2 prevented RLS extension; however, RLS extension was restored when both SIR2 and FOB1 were deleted in several cases, demonstrating that SIR2 is not directly required for RLS extension. These findings indicate that suppression of the sir2Δ lifespan defect is a rare phenotype among longevity interventions and suggest that sir2Δ cells senesce rapidly by a mechanism distinct from that of wild-type cells. They also demonstrate that failure to observe lifespan extension in a short-lived background, such as cells or animals lacking sirtuins, should be interpreted with caution. © 2011 The Authors. Aging Cell © 2011 Blackwell Publishing Ltd/Anatomical Society of Great Britain and Ireland.


Lu Y.,Guangdong Medical College | Lu Y.,Key Laboratory for Medical Molecular Diagnostics of Guangdong Province | Huang G.-L.,Guangdong Medical College | Huang G.-L.,Key Laboratory for Medical Molecular Diagnostics of Guangdong Province | And 9 more authors.
Molecular Biology Reports | Year: 2013

Peptidylprolyl cis/trans isomerase, NIMA-interacting 1 (PIN1) plays an important role in cell transformation and oncogenesis. Association between PIN1 promoter polymorphisms and cancer risk was reported in several cancers. This study aimed to evaluate the association between two single nucleotide polymorphisms (SNPs, -667T>C, rs2233679 and -842G>C, rs2233678) on PIN1 promoter and risk of nasopharyngeal carcinoma (NPC). The two SNPs were genotyped using polymerase chain reaction-restriction fragment length polymorphism in a total of 334 native Chinese subjects consisting of 178 cases and 156 controls. The results indicated that the -667CT heterozygote and -667CC homozygote exhibited a significantly decreased risk of nasopharyngeal carcinoma when compared with -667TT homozygote (OR = 0.639, 95 % CI = 0.452-0.903, p = 0.011 for -667CT; and OR = 0.441, 95 % CI = 0.213-0.915, p = 0.038 for -667CC, respectively). In the -842G>C polymorphism, compared with -842GG homozygote, only -842CG heterozygote but not -842CC homozygote had a significantly decreased risk of nasopharyngeal carcinoma (OR = 0.465, 95 % CI = 0.249-0.871, p = 0.010). Genotype in the two SNPs in patients showed no significant associations with the clinicopathologic features examined. Our study showed that the minor genotypes of PIN1 promoter (-667CT, -667CC and -842CG) were associated with decreased risk of NPC in a Chinese population, suggested that PIN1 promoter polymorphisms might play an important role in NPC carcinogenesis. © 2012 Springer Science+Business Media Dordrecht.


Huang H.,Southern Medical University | Wu Y.,Affiliated Hospital of Guangdong Medical University | Liao D.,Guangdong Medical University | Liao D.,Key Laboratory for Epigenetics of Dongguan City | And 2 more authors.
Minerva Medica | Year: 2016

INTRODUCTION: Previous studies about the possible link between genetic polymorphisms of interleukin-10 (IL-10) and nasopharyngeal carcinoma (NPC) risk offer controversial results, and the sample sizes recruited in these trials were relatively modest. To further determine this association, a comprehensive analysis was performed in the present study. EVIDENCE ACQUISITION: Eligible studies were selected from PubMed, Embase, Chinese National Knowledge Infrastructure (CNKI), China Biological Medicine Database and Wanfang Database. A total of 623 cases and 1,018 controls for the IL-10 -1082G/A polymorphism, 463 cases and 862 controls for the IL-10 -819T/C polymorphism, and 463 cases and 862 controls for the IL-10 -592A/C polymorphism were finally included in this meta-analysis. EVIDENCE SYNTHESIS: Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of the association by fixed-effects or random-effects models according to heterogeneity. In the present analysis, a strong relationship between the -1082G/A polymorphism in IL-10 promoter and NPC susceptibility was found in all genetic models [allele, 0.65 (0.45-0.94), P=0.02; co-dominant, 0.15 (0.06-0.38), P<0.0001;, dominant 14.37 (2.86-72.09), P=0.001; and recessive fashions, 0.56 (0.45-0.71), P<0.0001)]. However, NPC risk was linked to -592A/C or -819T/C polymorphism in IL-10 promoter only in the co-dominant model in both genetic situations [for -819T/C, 0.36 (0.17-0.78), P=0.01; for -592A/C, 0.39 (0.19-0.80), P=0.01]. CONCLUSIONS: Our study has shown that the IL-10 -1082G/A polymorphism might be associated with increased risk of NPC under all genetic models. However, NPC risk is linked to -592A/C or -819T/C polymorphism in IL-10 promoter only in the co-dominant model in both genetic situations. ©2016 Edizioni Minerva Medica.


Kaeberlein M.,University of Washington | Kaeberlein M.,Guangdong Medical College | Kennedy B.K.,Guangdong Medical College | Kennedy B.K.,Buck Institute for Research on Aging | And 5 more authors.
Mechanisms of Ageing and Development | Year: 2011

The " Trinations Aging Symposium" was held on the campus of Guangdong Medical College in Dongguan, China from April 28 to 30, 2011. The goal was to promote interaction, collaboration, and exchange of ideas between scientists in the field of aging research from Japan, South Korea, and China. Aging research is on the rise in Asia. This represents an important development, since Korea and Japan are the two longest-lived countries in the world, and life expectancy is increasing rapidly in China and other Asian countries. The world will see a greater percentage of people over age 65 in coming years than any period in human history. Developing therapeutic approaches to increase healthspan has the potential not only to enhance quality of life, but would also help stem the looming economic crisis associated with a high percentage of elderly. The focus of the Trinations Aging Symposium was on the basic biology of aging, and topics discussed included genome maintenance, metabolism and aging, longevity genes and interventions, and new therapies for age-related diseases. The meeting finished with a commitment for another symposium next year that will include additional Asian countries and the formation of a new scientific organization, the Asian Association for Aging Research. © 2011.


Liu B.,University of Hong Kong | Liu B.,Guangdong Medical College | Ghosh S.,University of Hong Kong | Yang X.,University of Hong Kong | And 16 more authors.
Cell Metabolism | Year: 2012

Abnormal splicing of LMNA gene or aberrant processing of prelamin A results in progeroid syndrome. Here we show that lamin A interacts with and activates SIRT1. SIRT1 exhibits reduced association with nuclear matrix (NM) and decreased deacetylase activity in the presence of progerin or prelamin A, leading to rapid depletion of adult stem cells (ASCs) in Zmpste24-/- mice. Resveratrol enhances the binding between SIRT1 and A-type lamins to increases its deacetylase activity. Resveratrol treatment rescues ASC decline, slows down body weight loss, improves trabecular bone structure and mineral density, and significantly extends the life span in Zmpste24-/- mice. Our data demonstrate lamin A as an activator of SIRT1 and provide a mechanistic explanation for the activation of SIRT1 by resveratrol. The link between conserved SIRT1 longevity pathway and progeria suggests a stem cell-based and SIRT1 pathway-dependent therapeutic strategy for progeria. © 2012 Elsevier Inc.


Huang G.-L.,Guangdong Medical College | Huang G.-L.,Key Laboratory for Medical Molecular Diagnostics of Guangdong Province | Chen M.-L.,Guangdong Medical College | Li Y.-Z.,Guangdong Medical College | And 12 more authors.
Journal of Human Genetics | Year: 2014

This case-control study focused on estimating the association between miR-146a polymorphism and risk of nasopharyngeal carcinoma (NPC) in central-south China. In total, 160 patients with NPC and 200 healthy controls in central-south China were genotyped using polymerase chain reaction-restriction fragment length polymorphism assay. Chi-square test was used to assess the different distribution of miR-146a polymorphism between NPC patients and controls; and logistic regression analysis was applied to analyze the associations between miR-146a polymorphism with cancer risk in different contrast models. Significant differences between NPC patients and controls were found in genotype (P=0.033 for GG versus CG versus CC; and odds ratio (OR)=0.568, 95% confidence interval (CI)=0.354-0.912, P=0.019 for CG versus CC; and OR=0.503, 95% CI=0.261-0.971, P=0.041 for CG versus CC; and OR=0.564, 95% CI=0.360-0.884, P=0.012 for GG+CG versus CC, respectively) and allelic analysis (P=0.025 for G versus C). Our findings suggested that polymorphism of mir-146a was associated with NPC in the central-southern Chinese population. © 2014 The Japan Society of Human Genetics All rights reserved 1434-5161/14.


Liao D.,Guangdong Medical College | Liao D.,Key Laboratory for Medical Molecular Diagnostics of Guangdong Province | Wu Y.,Guangdong Medical College | Wu Y.,Key Laboratory for Medical Molecular Diagnostics of Guangdong Province | And 13 more authors.
PLoS ONE | Year: 2014

Background: Cyclin D1 (CCND1) plays a key role in cell cycle regulation. It is a well-established human oncogene which is frequently amplified or overexpressed in cancers. The association between CCND1 G870A polymorphism and cancer risk has been widely assessed. However, a definitive conclusion between CCND1 G870A polymorphism and risk of nasopharyngeal carcinoma (NPC) remains elusive. Copyright:Methods: We firstly performed a hospital-based case-control study involving 165 NPC cases and 191 cancer-free controls in central-south China, and then conducted a meta-analysis with six case-control studies to evaluate the association between NPC risk and CCND1 G870A polymorphism.Results: The case-control study found a significant association between CCND1 G870A polymorphism and NPC risk in various comparison models (AA vs. GG: OR = 2.300, 95% CI 1.089-4.857, p = 0.029; AG vs. GG: OR = 2.832, 95% CI 1.367-5.867, p = 0.005; AA/AG vs. GG: OR = 2.597, 95% CI 1.288-5.237, p = 0.008; AA vs. AG/GG: OR = 0.984, 95% CI 0.638-1.518, p = 0.944). Further meta-analysis showed that there was no significant association between CCND1 G870A polymorphism and NPC risk in overall analysis. In the stratified analysis by race, however, significant associations were only found in Caucasians (for the allele model A vs. G: OR = 0.75, 95% CI 0.59-0.97, p = 0.03; for the co-dominant model AA vs. GG: OR = 0.52, 95% CI 0.32-0.86, p = 0.01; for the dominant model AA/AG vs. GG: OR = 0.49, 95% CI 0.32-0.74, p<0.01; for the recessive model AA vs. AG/GG: OR = 0.90, 95% CI 0.61-1.34, p = 0.60).Conclusions: A significant association between CCND1 G870A polymorphism and NPC risk was found in the centralsouthern Chinese population. The meta-analysis indicated that CCND1 G870A polymorphism may contribute to the development of NPC in Caucasians. © 2014 Liao et al.


Wang G.-H.,Guangdong Medical University | Huang G.-L.,Guangdong Medical University | Huang G.-L.,Key Laboratory for Medical Molecular Diagnostics of Guangdong Province | Zhao Y.,Guangdong Medical University | And 5 more authors.
Journal of Materials Chemistry B | Year: 2016

Stimuli-responsive nanocarriers for anticancer drug and gene co-delivery are a promising strategy in cancer therapy due to their combination of chemotherapy and gene therapy. In this work, we developed a facile and effective method to fabricate stimuli-responsive nanocarriers for anticancer drug and gene co-delivery based on complexes of polyethylenimine (PEI) with an adenosine triphosphate (ATP) responsive aptamer duplex (ARAD). No chemical reactions or complex modifications were used in the construction processes. In this system, Doxorubicin-loaded aptamer duplex and plasmid DNA (p53) can be bound by PEI by electronic interactions to form stable complexes which effectively protect the aptamer and p53 from DNase degradation. The intercalated Dox can be released on-demand by a structural change in the aptamer duplex in an ATP-rich environment. The morphology and average size of the nanocarriers were characterized by zeta potential and transmission electron microscopy (TEM). The nanocarriers exhibit lower cell toxicity in HeLa cell lines relative to PEI. RT-PCR and Western blot analysis confirmed that p53 could be effectively delivered and expressed in HeLa cells by PEI/ARAD/p53 complexes. Moreover, the apoptosis percentage of HeLa cells treated with PEI/ARAD/Dox/p53 complex increased to 40.8%, compared to 24.7% for PEI/ARAD/Dox complex and 11.5% for PEI/ARAD/p53, respectively. The result demonstrated that the combinatorial delivery of Dox and p53 by nanocarriers could induce synergistic actions and lead to effective cancer cell apoptosis. © 2016 The Royal Society of Chemistry.


Chen Y.-N.,Guangdong Medical University | Chen Y.-N.,Key Laboratory for Medical Molecular Diagnostics of Guangdong Province | Cai M.-Y.,Guangdong Medical University | Cai M.-Y.,Key Laboratory for Medical Molecular Diagnostics of Guangdong Province | And 14 more authors.
Oncotarget | Year: 2016

Long noncoding RNAs (lncRNAs) have gained extensive attentions in recent years because of their potential importance in a variety of biological and pathological processes. In this study, we sought to explore the role of lncRNAs in cellular senescence. Here, we report that the lncRNA AK156230 was downregulated during replicative senescence in mouse embryonic fibroblasts (MEFs), and knockdown of AK156230 promotes a robust senescence phenotype, including increase in the numbers of the senescence-associated β-galactosidase-positive cells, decrease of cell proliferation, accumulation of cells in the G2/M phase and reduction of autophagic activity. The cells with knockdown AK156230 expression also exhibited increased levels of p21, p53 and phosphorylated p53, and a decreased activity of CDK1. Moreover, rapamycin-induced autophagy offered cytoprotective effect and rescued cellular senescence in AK156230 knockdown cells. Gene expression profile showed that the dysregulation of autophagy and cell cycle genes contributed to the induction of cellular senescence after AK1561230 silencing. Taken together, these results suggest that downregulation of AK156230 is involved in the induction of cellular senescence through its roles in autophagy and cell cycle progression. Our study identifies AK156230 as a critical lncRNA that has a role in regulating cellular senescence in MEFs.

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