Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics

Dongguan, China

Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics

Dongguan, China
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Zuo C.,Guangdong Medical College | Wang Z.,Guangdong Medical College | Wang Z.,Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics | Lu H.,Guangdong Medical College | And 4 more authors.
Molecular Medicine Reports | Year: 2013

Protein-coding genes and small non-coding microRNAs involved in the guidance of differentiation in mesenchymal stem cells (MSCs) into osteoblasts have been extensively investigated in previous studies. However, long non-coding RNAs (lncRNAs), which account for a large proportion of the genomic sequences in numerous species, have not yet been reported. In the present study, the lncRNA expression profile was analyzed using the Arraystar lncRNA array in C3H10T1/2 MSCs undergoing early osteoblast differentiation and 116 differentially expressed lncRNAs were identified between BMP-2 treated and untreated groups. Among these lncRNAs, 59 were upregulated and 57 were downregulated in BMP-2 treated groups. In addition, 24 cooperatively differentially expressed lncRNAs and nearby mRNA pairs were found. For example, mouselincRNA0231 and its nearby gene, EGFR, were downregulated, while lncRNA NR-027652 and its nearby gene, DLK1, were upregulated. These observations may be part of the regulatory mechanisms of lncRNAs in the control of osteoblast differentiaton. In conclusion, results of the present study indicate that lncRNA expression profiles are significantly altered in C3H10T1/2 undergoing early osteoblast differentiation and these results may provide insight into the mechanisms responsible for osteoblast differentiation.


Li S.,Guangdong Medical College | Li S.,Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics | Zhang Y.,Guangdong Medical College | Xu J.,Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics | And 7 more authors.
Applied Physics Letters | Year: 2014

This study aims to present a noninvasive prostate cancer screening methods using serum surface-enhanced Raman scattering (SERS) and support vector machine (SVM) techniques through peripheral blood sample. SERS measurements are performed using serum samples from 93 prostate cancer patients and 68 healthy volunteers by silver nanoparticles. Three types of kernel functions including linear, polynomial, and Gaussian radial basis function (RBF) are employed to build SVM diagnostic models for classifying measured SERS spectra. For comparably evaluating the performance of SVM classification models, the standard multivariate statistic analysis method of principal component analysis (PCA) is also applied to classify the same datasets. The study results show that for the RBF kernel SVM diagnostic model, the diagnostic accuracy of 98.1% is acquired, which is superior to the results of 91.3% obtained from PCA methods. The receiver operating characteristic curve of diagnostic models further confirm above research results. This study demonstrates that label-free serum SERS analysis technique combined with SVM diagnostic algorithm has great potential for noninvasive prostate cancer screening. © 2014 AIP Publishing LLC.


Li S.,Guangdong Medical College | Li S.,Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics | Chen G.,Sun Yat Sen University | Zhang Y.,Guangdong Medical College | And 5 more authors.
Optics Express | Year: 2014

This study aims to detect colorectal cancer with near-infrared Raman spectroscopy and feature selection techniques. A total of 306 Raman spectra of colorectal cancer tissues and normal tissues are acquired from 44 colorectal cancer patients. Five diagnostically important Raman bands in the regions of 815-830, 935-945, 1131-1141, 1447-1457 and 1665-1675cm-1 related to proteins, nucleic acids and lipids of tissues are identified with the ant colony optimization (ACO) and support vector machine (SVM). The diagnostic models built with the identified Raman bands provide a diagnostic accuracy of 93.2% for identifying colorectal cancer from normal Raman spectroscopy. The study demonstrates that the Raman spectroscopy associated with ACO-SVM diagnostic algorithms has great potential to characterize and diagnose colorectal cancer. © 2014 Optical Society of America.


PubMed | Chinese Institute of Clinical Medicine, Dongguan 5th Hospital, Affiliated Hospital of Guangdong Medical University, Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics and University of Maryland Baltimore County
Type: | Journal: Mediators of inflammation | Year: 2016

Recent studies suggest that tumor-associated macrophage-produced IL-6 is an important mediator within the tumor microenvironment that promotes tumor growth. The activation of IL-6/STAT3 axis has been associated with chemoresistance and poor prognosis of a variety of cancers including colorectal carcinoma and thus serves as a potential immunotherapeutic target for cancer treatment. However, it is not fully understood whether anticytokine therapy could reverse chemosensitivity and enhance the suppressive effect of chemotherapy on tumor growth. In this study, we aimed to investigate the effect of IL-6 inhibition therapy on the antitumor effect of carboplatin. Enhanced expression of IL-6 and activation of STAT3 were observed in human colorectal carcinoma samples compared to normal colorectal tissue, with higher levels of IL-6/STAT3 in low grade carcinomas. Treatment of carboplatin (CBP) dose-dependently increased IL-6 production and STAT3 activation in human colorectal LoVo cells. Blockade of IL-6 with neutralizing antibody enhanced chemosensitivity of LoVo cells to carboplatin as evidenced by increased cell apoptosis. IL-6 blockade abolished carboplatin-induced STAT3 activation. IL-6 blockade and carboplatin synergistically reduced cyclin D1 expression and enhanced caspase-3 activity in LoVo cells. Our results suggest that inhibition of IL-6 may enhance chemosensitivity of colon cancers with overactive STAT3 to platinum agents.


Xu D.,Guangzhou University | Wang J.,Guangzhou University | Zhou Z.,South China University of Technology | He Z.,Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics | Zhao Q.,Guangzhou University
Molecular Medicine Reports | Year: 2015

Hepatocellular carcinoma (HCC) is the leading cause of cancer-associated mortality worldwide; however, only limited therapeutic treatments are currently available. The present study aimed to investigate the effects of cannabinoids as novel therapeutic targets in HCC. In addition, the mechanism underlying the effects of a synthetic cannabinoid, WIN55, 212-2, on the BEL7402 HCC cell line was investigated. The results demonstrated that WIN55, 212-2 induced cell cycle arrest of the BEL7402 cells at the G0/G1 phase via cannabinoid receptor 2 (CB2) mediated downregulation of phosphorylated-extracellular signal-regulated kinases (ERK)1/2, upregulation of p27, and downregulation of cyclin D1 and cyclin-dependent kinase 4. Furthermore, inhibition of CB2 with the CB2 antagonist AM630 abrogated WIN55, 212-2-induced cell cycle arrest. Inhibition of ERK1/2 also resulted in cell cycle dysregulation and cell cycle arrest at the G0/G1 phase, which subsequently resulted in cell growth inhibition. In addition, the present study detected a significant reduction in matrix metalloproteinase-9, retinoblastoma protein and E2F1 expression, and migration inhibition by WIN treatment. These results suggested that cannabinoid receptor agonists, including WIN, may be considered as novel therapeutics for the treatment of HCC.


PubMed | Guangzhou University, South China University of Technology and Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics
Type: Journal Article | Journal: Molecular medicine reports | Year: 2015

Hepatocellular carcinoma (HCC) is the leading cause of cancer-associated mortality worldwide; however, only limited therapeutic treatments are currently available. The present study aimed to investigate the effects of cannabinoids as novel therapeutic targets in HCC. In addition, the mechanism underlying the effects of a synthetic cannabinoid, WIN55, 2122, on the BEL7402HCC cell line was investigated. The results demonstrated that WIN55, 2122 induced cell cycle arrest of the BEL7402 cells at the G0/G1 phase via cannabinoid receptor2(CB2)mediated downregulation of phosphorylated-extracellular signal-regulated kinases (ERK)1/2, upregulation of p27, and downregulation of cyclinD1and cyclindependent kinase4. Furthermore, inhibition of CB2with the CB2antagonist AM630abrogated WIN55, 2122induced cell cycle arrest. Inhibition of ERK1/2also resulted in cell cycle dysregulation and cell cycle arrest at the G0/G1phase, which subsequently resulted in cell growth inhibition. In addition, the present study detected a significant reduction in matrix metalloproteinase9, retinoblastoma protein and E2F1expression, and migration inhibition by WIN treatment. These results suggested that cannabinoid receptor agonists, including WIN, may be considered as novel therapeutics for the treatment of HCC.


Xiong X.-D.,Guangdong Medical College | Xiong X.-D.,Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics | Xiong X.-D.,Shantou University | Luo X.-P.,Guangdong Women and Children Hospital and Health Institute | And 6 more authors.
Gynecologic Oncology | Year: 2014

Objective MicroRNAs (miRNAs) play critical roles in cervical carcinogenesis. Common single nucleotide polymorphisms (SNPs) in pre/pri-miRNAs may change their property through altering miRNAs expression and/or maturation. Here we aimed to investigate the influence of three common SNPs in pre/pri-miRNAs (pri-miR-26a-1 rs7372209, pre-miR-27a rs895819 and pri-miR-100 rs1834306) on individual susceptibility to cervical cancer. Methods We genotyped these three polymorphisms in 103 cervical cancer cases and 417 cancer-free female subjects using polymerase chain reaction-ligation detection reaction (PCR-LDR) method. Unconditional logistic regression analysis was utilized to estimate the association between these polymorphisms and the risk of cervical cancer. Results In a logistic regression analysis, we found that the rs895819 polymorphism in pre-miR-27a exhibited a significant effect on cervical cancer risk; T allele (OR = 0.68, 95% CI = 0.49-0.95, P = 0.025), and CT (OR = 0.33, 95% CI = 0.15-0.74, P = 0.007) or TT (OR = 0.33, 95% CI = 0.15-0.72, P = 0.006) genotype were associated with the decreased risk, compared to C and CC respectively. As we used further genotype association models, we found a similar trend of the association in additive (OR = 0.70, P = 0.041) and recessive model (OR = 0.33, P = 0.004). We did not detect any association of the other two SNPs in pri-miR-26a-1 (rs7372209) and pri-miR-100 (rs1834306) with cervical cancer risk. Conclusion Our study provides the first evidence that the miR-27a rs895819 polymorphism is associated with a decreased risk of cervical cancer in southern Chinese women. © 2013 Elsevier Inc. All rights reserved.


Xiong X.-D.,Guangdong Medical College | Xiong X.-D.,Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics | Cho M.,Yeshiva University | Cai X.-P.,Guangdong Medical College | And 11 more authors.
Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis | Year: 2014

miRNAs are small non-coding RNAs that play an important role in numerous physiological processes. Common single nucleotide polymorphisms (SNPs) in pre-miRNAs may change their property through altering miRNAs expression and/or maturation, resulting in diverse functional consequences. To date, the role of genetic variants in pre-miRNAs on coronary artery disease (CAD) risk remains poorly understood. Here we aimed to evaluate the influence of three common SNPs in pre-miRNAs (miR-146a rs2910164 G>C, miR-196a2 rs11614913 C>T, miR-499 rs3746444 T>C) on individual susceptibility to CAD in a Chinese population of 295 CAD patients and 283 controls. Genotyping was performed using polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP) method. In a logistic regression analysis, we detected an association of rs2910164 in pre-miR-146a with the CAD risk; compared with the GG homozygotes, the GC heterozygotes [odds ratio (OR)=1.89, 95% confidence interval (CI)=1.06-3.36, P=0.029] and the CC homozygotes (OR=1.83, 95% CI=1.01-3.32, P=0.046) genotype were statistically significantly associated with the increased risk for CADs. As we used further genotype association models, we found a similar trend of the association in recessive model (OR=1.86, 95% CI=1.09-3.19, P=0.023). We also found that the genotypes of miR-146a rs2910164 were associated with its mature miRNA expression by analyzing 23 PBMC samples from CAD patients. Individuals carrying rs11614913 GC or CC genotypes showed 3.2-fold higher expression compared to GG genotype carriers (P<. 0.05). We observed no association of the other two SNPs in miR-196a2 (rs11614913) and miR-499 (rs3746444) with the CAD incidence. Our data provide the first evidence that the miR-146a rs2910164 polymorphism is associated with increased risk of CAD in Chinese Han population, which may be through influencing the expression levels of the miRNA. © 2014 Elsevier B.V.


Chen Y.-N.,Guangdong Medical College | Chen Y.-N.,Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics | Xiong X.-D.,Guangdong Medical College | Xiong X.-D.,Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics
Progress in Biochemistry and Biophysics | Year: 2014

There is a growing interest for epigenetics in recent years. The main patterns of epigenetic regulation include DNA methylation, histone modification and chromatin remodeling, etc. The outcome of ENCODE project and subsequent studies have revealed that only a small portion of human genome encodes proteins, while the vast majority are transcribed as non-coding RNA (ncRNA). Long non-coding RNA (lncRNA) is commonly defined as an RNA molecule which is larger than 200 nucleotides (nt) and not translated into proteins. Growing evidences have suggested that lncRNAs can regulate gene expression at various levels including epigenetic regulation, transcriptional regulation and post-transcriptional regulation, and are involved in a wide variety of biological processes, such as cell proliferation, differentiation and apoptosis. In this review, we highlight the recent advances of howlncRNAs function in the epigenetic regulation.


PubMed | Guangdong Medical College and Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics
Type: Journal Article | Journal: Oncology reports | Year: 2016

In the present study, we aimed to investigate the effects of CC chemokine ligand 22 (CCL22) and interleukin-37 (IL-37) on the proliferation and epithelial-mesenchymal transition (EMT) of non-small cell lung cancer (NSCLC) A549 cells. pDsRed-CCL22 and pEGFP-IL-37 plasmids were constructed. A549 cells were divided into six groups: the control, the pDsRed-N1 blank plasmid, the pEGFP-C1 blank plasmid, the pDsRed-CCL22 plasmid, the pEGFPIL-37 plasmid and the pDsRed-CCL22+pEGFP-IL-37 plasmid group. Expression levels and localization of CCL22 and IL-37 in cells were detected by confocal microscopy. Phase-contrast microscopy was applied for observing cellular morphology. Real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) was used for detecting the mRNA levels of vimentin, N-cadherin and E-cadherin, and their protein expression levels were tested using western blotting. Constructed plasmids expressed CCL22 and IL-37, both of which had a co-localization in the cell membrane. MTT assay and cell observation results revealed that CCL22 and IL-37 inhibited the proliferation and EMT process of the A549 cells. The results of RT-qPCR and western blotting revealed that decreased vimentin and N-cadherin mRNA and protein expression levels, and increased E-cadherin mRNA and protein expression levels were found in the pDsRed-CCL22 plasmid, pEGFP-IL-37 plasmid and pDsRedCCL22+pEGFPIL-37 plasmid groups when compared with the control, the pDsRed-N1 blank plasmid and the pEGFP-C1 blank plasmid groups (all P<0.05), and decreased vimentin and N-cadherin mRNA and protein expression levels and increased E-cadherin mRNA and protein expression levels were found in the pDsRedCCL22+pEGFPIL-37 plasmid group when compared with the pDsRed-CCL22 plasmid and the pEGFPIL-37 plasmid groups (all P<0.05). CCL22 and IL-37 with a co-localization in the A549 cells inhibited the proliferation and EMT process in A549 cells. The antitumor effects of CCL22 and IL37 provide a strategy for the treatment of NSCLC.

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