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ABSTRACT: Abstract Objective. MicroRNA-133a (miR-133a) and microRNA-133b (miR-133b) are located on chromosome 18 in the same bicistronic unit. Recently, they have been commonly identified as being down-regulated in various human malignancies, such as bladder cancer, pancreatic ductal adenocarcinoma, oesophageal squamous cell carcinoma of the tongue, and hepatocellular and lung carcinomas. The present study examined the effects of miR-133a and miR-133b in bladder cancer T24 and EJ cells. Material and methods. After transfection of miR-133a and miR-133b, the expression of miR-133a/b was assessed, and a cell viability assay, cell migration assay, cell invasion assay, luciferase assay and Western blot were conducted in bladder cancer T24 and EJ cells. Results. Both miR-133a and miR-133b were found to inhibit cell proliferation, migration and invasion in T24 and EJ cells. The first evidence was provided that miR-133a and miR-133b may directly target the epidermal growth factor receptor in bladder cancer. Conclusions. This study provided the first glimpse of the functional role of miR-133 in bladder cancer T24 and EJ cells. The results may increase our knowledge on the molecular basis of progression and provide potential therapy for bladder cancer.
Scandinavian Journal of Urology and Nephrology 12/2012; · 0.99 Impact Factor
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ABSTRACT: Numerous studies have suggested that interleukin 11 (IL-11) has roles in human gastric, prostate and bone cancer and endometrial carcinoma. Hence, we evaluated the expression of IL-11 in bladder cancer and the correlation of IL-11 levels and clinico-pathological features. The expression of IL-11 in primary human bladder cell culture, human bladder cancer cell lines, transitional cell carcinoma (TCC) and non-cancerous bladder tissues (NATs) were analyzed by western blotting. Enzyme-linked immunosorbent assay (ELISA) for urinary IL-11 was performed to compare the IL-11 levels in healthy subjects and subjects diagnosed with bladder cancer. Our study suggested that the expression of IL-11 in human bladder cancer cell lines and TCC was downregulated compared with primary human bladder cell culture and matched NATs. We also demonstrated reduced urinary levels of IL-11 in subjects with bladder cancer compared with healthy subjects. Furthermore, we revealed that the levels of IL-11 were associated with tumor grade and stage. The results suggested that reduced levels of IL-11 may play an important role in the carcinogenesis and progression of TCC. They also indicated that IL-11 may be a promising predictor for prognosis of TCC.
Molecular Medicine Reports 11/2012; · 0.42 Impact Factor
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ABSTRACT: It has been shown that regulation of EGFR expression in prostate cancer cells is mostly at the transcriptional level. microRNA-133 (miR-133) has long been recognized as a muscle-specific miRNA which may regulate myoblast differentiation and participate in many myogenic diseases. Recently, it has been reported that miR-133 is also involved in other tumors, such as bladder cancer, esophageal cancer and may regulate cell motility in these cancer cells. In the present study, we examined the expression and effects of miR-133 in two hormone-insensitive prostate cancer cell lines. The expression of miR-133a and miR-133b were analyzed by quantitative RT-PCR. After transfection of miR-133a and miR-133b, cell viability assay, luciferase assay, western blot analysis, cell migration and invasion assay were conducted in Du145 and PC3 cells. In this study, we showed that miR‑133a and miR-133b are expressed at the detection limit in two hormone-insensitive prostate cancer cell lines, PC3 and DU145. Ectopic expression of miR-133 inhibited cell proliferation, migration and invasion in these cells. We also provide the first evidence that miR-133 may target EGFR. Our study provided the first glimpse of the functional role of miR-133 in two hormone-independent prostate cancer cell lines. These results may add to our knowledge on the molecular basis of prostate cancer progression.
Oncology Reports 03/2012; 27(6):1967-75. · 1.84 Impact Factor
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ABSTRACT: A newly created multivitamin possesses many protective health functions. To investigate its safety when applied in medical treatment and when used as a food supplement, we studied its acute oral toxicity and 13-week oral toxicity in mice. The results showed that the oral lethal dose, 50% (LD(50)) of the biomass of the multivitamin in mice was greater than 2492 mg/kg body weight (BW) and that poisoned mice recovered within 72 h. The no observed effect level (NOEL) of long-term consumption was more than 249.3mg/kg BW for haematological parameters, clinical chemistry parameters, histopathological examination of organs, food consumption, BW, ratio of organ weight to BW and other physiological parameters and conditions. Therefore, we conclude that dosages of up to 249.3 mg/kg BW/day of this multivitamin do not cause chronic toxicity in animals. Administration of this multivitamin may even improve the resistance of animals to negative environmental factors and may be safe for long-term consumption to enhance the health of individuals in accordance with the prescribed dosage (1.4 ∼ 4.2 mg/kg BW/day).
Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 03/2012; 50(5):1776-80. · 2.99 Impact Factor
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ABSTRACT: Correlation between molecular structures and slow relaxation of magnetization of three mixed (phthalocyaninato)(porphyrinato) dysprosium(III) double-deckers clearly reveals the effect of the sandwich-type molecular structure, in particular the twist angle, on the quantum tunneling (QT) at zero dc field of these complexes, providing the first direct evidence to the theoretical inference.
Chemical Communications 02/2012; 48(24):2973-5. · 6.17 Impact Factor
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ABSTRACT: Despite advancements in research made over the past decades, the prognosis of gliomas remains dismal. Fas/Fas ligand (Fas-L)-related immunotherapy may be regarded as a treatment of choice as it can induce the apoptosis of glioma cells, and has shown promising results in experimental studies. Over the years, brain glioma stem cells (BGSCs) have been accepted as the origin of gliomas and determine their biological features. The theory of BGSCs has facilitated the study of gliomas. In this study, we conducted a series of assays to culture BGSCs from clinical samples and determined the mRNA expression levels of Fas/Fas-L in BGSCs. We also investigated the effects of Fas/Fas-L-related immunotherapy on the apoptosis of glioma cells. BGSCs were grown from samples of 8 patients suffering from gliomas and identified by the assessment of biological characteristics and immunocytochemistry. Total RNA was extracted and reverse-transcribed into cDNA, and the expression levels of Fas/Fas-L mRNA were determined by real-time RT-PCR, followed by statistical analysis. The results showed that the Fas and Fas-L mRNA expression levels in BGSCs were lower compared to those in primary cultured glioma cells, which were statistically significant (P<0.001). These results indicate that immunotherapy involving Fas/Fas-L may not eradicate the BGSCs, which would result in the relapse of glioma. However, further research is required to investigate the mechanisms involved and define the prospect of Fas-involved immunotherapy against gliomas.
Molecular Medicine Reports 02/2012; 5(5):1202-6. · 0.42 Impact Factor
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ABSTRACT: Although endothelial progenitor cells (EPCs) play a pivotal role in the endothelial repair following arterial injury and shear stress has a beneficial effect on EPCs, however, the molecular mechanism underlying the influence of EPCs on the endothelial integrity and the regulation of shear stress on the EPC signaling remained to be studied. Here, we investigated the effects of laminar shear stress on the tyrosine kinase with immunoglobulin and epidermal growth factor homology domain-2 (Tie2)-dependent signaling and its relation to in vivo reendothelialization capacity of human early EPCs. The human early EPCs were treated with shear stress. Shear stress in a dose-dependent manner increased angiopoietin-2 (Ang2)-induced migratory, adhesive and proliferatory activities of EPCs. Transplantation of EPCs treated by shear stress facilitated in vivo reendothelialization in nude mouse model of carotid artery injury. In parallel, the phosphorylation of Tie2 and Akt of EPCs in response to shear stress was significantly enhanced. With treatment of Tie2 knockdown or Akt inhibition, shear stress-induced phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) of EPCs was markedly suppressed. After Tie2/PI3K/Akt/eNOS signaling was blocked, the effects of shear stress on in vitro function and in vivo reendothelialization capacity of EPCs were significantly inhibited. The present findings demonstrate for the first time that Tie2/PI3k/Akt/eNOS signaling pathway is, at least in part, involved in the EPCs-mediated reendothelialization after arterial injury. The upregulation of shear stress-induced Tie2-dependent signaling contributes to enhanced in vivo reendothelialization capacity of human EPCs.
Journal of Molecular and Cellular Cardiology 02/2012; 52(5):1155-63. · 5.17 Impact Factor
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ABSTRACT: Dysregulation of microRNA metabolism has been observed in a variety of human cancers. In this study, we evaluated the expression of the enzymes of the machinery Dicer, Drosha and DGCR8, in transitional cell carcinomas (TCCs) of the urinary bladder. The expression of Dicer, Drosha and DGCR8 was analyzed using semi-quantitative RT-PCR in clinical specimens from normal bladder mucosa, TCCs and their normal adjacent tissues (NATs). Immunohistochemistry was performed to compare the expression of Dicer in normal, TCCs and NATs. Our study demonstrated that Dicer mRNA levels in TCCs were significantly lower compared to normal samples and NAT samples. The immunohistochemistry results revealed that Dicer protein levels in TCCs were significantly downregulated compared to normal bladder mucosa and NATs. Our data demonstrated that Dicer is significantly downregulated in TCCs compared to paired NAT samples and normal samples, suggesting that reduced expression of Dicer may play an important role in bladder cancer.
Molecular Medicine Reports 12/2011; 5(3):695-9. · 0.42 Impact Factor
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Bin Xu,
Ning Wang,
Xuhui Wang,
Na Tong,
Ning Shao, Jun Tao,
Pengchao Li,
Xiaobing Niu,
Ninghan Feng,
Lihua Zhang,
Lixin Hua,
Zengjun Wang,
Ming Chen
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ABSTRACT: Castration-resistant prostate cancer (CRPC) is a leading cause of cancer-related deaths in elder men. This disease has limited therapeutic options and poor prognosis as the underlying molecular mechanisms are not clearly understood. Given the emerging roles of microRNA (miRNA) as a key regulator, we postulated that miRNA may play a significant role in CRPC formation.
miR-146a levels in 15 androgen-dependent prostate cancer (ADPC) tissues and 5 CRPC tissues were measured by qRT-PCR. Effects of miR-146a in cell proliferation and migration in vitro and in vivo were evaluated by MTT assay, colony formation assay, transwell migratory assay, and tumor formation assay, respectively.
we found that miR-146a expression was significantly decreased in CRPC tissues compared to ADPC tissues. Functional analyses showed that ectopic overexpression of miR-146a in androgen-independent cell lines not only inhibited cell growth, colony formation, and migration in vitro, but also reduced tumorigenicity and angiogenesis in vivo. Mechanistic studies revealed that miR-146a repressed the expression of EGFR through binding to its 3'-untranslated region. Also, miR-146a inhibited the expression of MMP2, one of the most important genes in tumor progression. Moreover, downregulation of p-ERK expression significantly abrogated miR-146a-induced prostate cancer cell proliferation.
Our findings suggest that ubiquitous loss of miR-146a is a critical mechanism for overexpression of EGFR in CRPC, which is crucial to better understanding the pathogenesis of CRPC.
The Prostate 12/2011; 72(11):1171-8. · 3.48 Impact Factor
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ABSTRACT: The miR-17-92 cluster has long been recognized as an oncogenic microRNA (miRNA) cluster and is amplified in multiple cancers. However, the individual roles of its members in carcinogenesis are largely undetermined. After transfection of miR-18a mimics, an antisense oligonucleotides inhibitor, siRNAs and a luciferase reporter plasmid, the MTT assay, colony formation assay, semi-quantitative RT-PCR, luciferase assay and Western blot analysis were conducted in bladder cancer cells. In the present study, we showed that miR-18a, a member of the miR-17-92 cluster, suppressed cell proliferation in bladder cancer T24 cells. Furthermore, ectopic expression of miR-18a in T24 cells down-regulated Dicer expression at both the mRNA and protein level, while inhibition miR-18a by antisense oligonucleotides could enhance Dicer expression in T24 cells. Two binding sites of miR-18a were found in Dicer 3' untranslated region (3' UTR). Luciferase reporter assay demonstrated that both sites could mediate expression suppression in vitro. In addition, knockdown of Dicer expression by siRNA mimicked cell growth suppression induced by miR-18a in T24 cells. These results show that miR-18a functions as a tumor suppressor by targeting Dicer in bladder cancer T24 cells and revealed a noteworthy feedback loop, which may be utilized by the miR-17-92 cluster to control miRNA output and prevent its overexpression.
Molecular Medicine Reports 09/2011; 5(1):167-72. · 0.42 Impact Factor
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ABSTRACT: Phosphatidylinositol 3-kinase (PI3K)-AKT signaling is a well-characterized pathway involved in the control of cell proliferation, apoptosis and oncogenesis. LY294002 is a commonly used pharmacologic inhibitor which acts at the ATP-binding site of the PI3K enzyme, thus selectively inhibiting the PI3K-AKT nexus. The purpose of the present study was to examine whether PI3K inhibited by LY294002 had an effect on human bladder cancer cells.
After treatment with LY294002, MTT assay, chemosensitivity test, colony formation assay, apoptosis assay and Western blot analysis were conducted in EJ cells.
EJ cells treated with LY294002 showed significant AKT phosphorylation suppression in a dose-response manner. Also, PI3K/AKT signaling inhibitor LY294002 suppressed cell proliferation and enhanced the chemosensitivity of doxorubicin in human bladder cancer EJ cells. Furthermore, LY294002 increased cell apoptosis to doxorubicin.
The augmentation of doxorubicin with PI3K inhibitor LY294002 may resolve the multidrug resistance of bladder cancer, and this may be a new strategy for achieving tolerance for chemotherapeutic agents in bladder cancer therapy.
Urologia Internationalis 05/2011; 87(1):105-13. · 0.99 Impact Factor
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Ninghan Feng,
Bin Xu, Jun Tao,
Pengchao Li,
Gong Cheng,
Zhichao Min,
Yuanyuan Mi,
Meilin Wang,
Na Tong,
Jialin Tang,
Zhengdong Zhang,
Hongfei Wu,
Wei Zhang,
Zengjun Wang,
Lixin Hua
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ABSTRACT: Recently, a C>T polymorphism (rs1434536) in a miR-125b binding site in the 3' untranslated region (3'UTR) of bone morphogenetic protein membrane receptor type IB gene (BMPR1B) has been found to contribute to cancer susceptibility. To investigate whether it plays an important role in the development of prostate cancer in southern Chinese Han population, we performed a case-control study. 247 prostate cancer and 278 control subjects were included in the cancer association study and dual-luciferase reporter assay was used to test the binding ability of miR-125b to BMPR1B-C or -T vectors. The effect of CT/TT genotype on prostate cancer risk was found to be significant for localized disease (OR=1.60, 95% CI=1.01-2.53, P=0.044) and among subgroups of aged>70 years (OR=1.90, 95% CI=1.15-3.15, P=0.015) compared with CC genotype. Moreover, C-allele gave a reduced luciferase activity relative to T-allele in dual-luciferase reporter assay. Our findings show that rs1434536 in the 3'UTR of BMPR1B gene affects the binding ability of miR-125b to BMPR1B mRNA and contributes to the genetic predisposition to localized prostate cancer and patients aged>70 years.
Molecular Biology Reports 05/2011; 39(1):369-73. · 2.93 Impact Factor
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ABSTRACT: Transitional cell carcinomas (TCCs) of the urinary bladder are common malignancies with a high recurrence rate. Since microRNA-21 (miR-21) may contribute to tumorigenesis and chemoresistance in many cancer types, we aimed to investigate its efficacy in TCCs. The expression of miR-21 and its target PTEN was determined by real-time qRT-PCR and western blotting, respectively in tumor tissues as well as adjacent non-tumor mucosa. The effect of miR-21 on cell proliferation and chemosensitivity to doxorubicin were measured using the MTT method. Cell apoptosis induced by doxorubicin was investigated using flow cytometry in the T24 cell line. BCL-2, AKT and pAKT were detected by western blotting for analysis of potential mechanisms. miR-21 was significantly up-regulated in tumor tissues while PTEN was expressed in lower levels compared to non-tumor tissues. A negative correlation between expression of miR-21 and PTEN was established in vivo. Cell proliferation and chemoresistance to doxorubicin were promoted by overexpression of miR-21 in T24 cells. BCL-2 up-regulation could be achieved by miR-21 overexpression, which prevented T24 cells from apoptosis induced by doxorubicin. Furthermore, the miR-21 induced BCL-2 up-regulation could be cancelled by the PI3K inhibitor LY294002. These data verified the oncogenic role of miR-21 in TCCs and may usher in new therapeutic strategies in treating this disease.
Oncology Reports 04/2011; 25(6):1721-9. · 1.84 Impact Factor
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Bin Xu,
Xiaobing Niu,
Xiangxiang Zhang, Jun Tao,
Deyao Wu,
Zidun Wang,
Pengchao Li,
Wei Zhang,
Hongfei Wu,
Ninghan Feng,
Zengjun Wang,
Lixin Hua,
Xinru Wang
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ABSTRACT: MicroRNAs have been implicated in regulating diverse cellular pathways. Emerging evidence indicates that miR-143 plays causal roles in cancer tumorigenesis as a tumor suppress gene; however, its role in prostate cancer tumorigenesis remains largely unknown. The aims of this study were to verify the effect of miR-143 on proliferation and migration abilities of prostate cancer cells. The expression level of miR-143 and its target gene KRAS were measured by realtime PCR and western blotting, respectively. Effects of miR-143 in cell proliferation, migration and chemosensitivity were evaluated by MTT assay, FACS cell cycle analysis, colony formation assay, and transwell migratory assay. Our results revealed an inverse correlation of expression between miR-143 and KRAS protein in prostate cancer samples (Pearson's correlation scatter plots: R = -0.707, P < 0.05). Moreover, over-expression of miR-143 in prostate cancer cells suppressed their proliferation and migration and increased their sensitivity to docetaxel by targeting EGFR/RAS/MAPK pathway. These findings suggest that miR-143 plays an important role in prostate cancer proliferation, migration and chemosensitivity by suppressing KRAS and subsequent inactivation of MAPK pathway, which provides a potential development of a new approach for the treatment of prostate cancer.
Molecular and Cellular Biochemistry 01/2011; 350(1-2):207-13. · 2.06 Impact Factor
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Bin Xu,
Xiao-Bing Niu,
Zi-Dun Wang,
Wei Cheng,
Na Tong,
Yuan-Yuan Mi,
Zhi-Chao Min, Jun Tao,
Peng-Chao Li,
Wei Zhang,
Hong-Fei Wu,
Zheng-Dong Zhang,
Zeng-Jun Wang,
Li-Xin Hua,
Ning-Han Feng,
Xin-Ru Wang
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ABSTRACT: Interleukin-6 (IL-6) is a multifunctional cytokine involved in different physiologic and pathophysiologic processes and plays important roles in the etiology of cancer. The -174G>C polymorphism of the IL-6 gene influences IL-6 transcription and has been implicated in cancer risk. However, published data have been conflicting. To derive a more precise estimation of the relationship, a meta-analysis of 29,377 cancer cases and 37,739 controls from 50 published case-control studies was performed. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated to assess the association between -174G>C polymorphism and cancer risk. Overall meta-analysis indicated that no association was found between -174G>C genotypes and cancer risk. However, the positive association was found in bladder cancer (OR=4.33, 95% CI: 1.93-9.71 for CC vs. GC, OR=2.81, 95% CI: 1.39-5.68 for CC vs. GG, and OR=2.19, 95% CI: 1.32-3.64 for CC vs. GG/GC), and among Asians (OR=2.08, 95% CI: 1.07-4.06 for CC vs. GG, and OR=2.20, 95% CI: 1.02-4.74 for CC vs. GG/GC) and Africans (OR=1.61, 95% CI: 1.07-2.42 for GC vs. GG). This meta-analysis showed the evidence that the -174G>C of the IL-6 gene was a low-penetrance susceptibility gene for bladder cancer. Further larger, preferably prospective studies are needed to confirm this relationship.
Molecular Biology Reports 11/2010; 38(4):2589-96. · 2.93 Impact Factor
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Bin Xu,
Zheng Xu,
Gong Cheng,
Zhi-Chao Min,
Yuanyuan Mi,
Zhi-zhong Zhang, Jun Tao,
Peng-Chao Li,
Mei-Lin Wang,
Jia-Lin Tang,
Zheng-Dong Zhang,
Wei Zhang,
Hong-Fei Wu,
Ning-Han Feng,
Li-Xin Hua
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ABSTRACT: Alterations in the TP53 and MDM2 genes appear to be important in the development of many human tumors, but evidence is conflicting on associations between polymorphisms in these genes and risk of prostate cancer (PCa). The influence of TP53 codon 72, MDM2 SNP309, and MDM2 C1797G polymorphisms in southern Chinese PCa patients was investigated. In the comparison of genotype distributions of TP53 codon 72 between cases and controls, the adjusted odds ratios for PCa associated with the Pro/Pro, Arg/Pro, and Arg/Arg genotypes were 1.00, 1.89 (95% CI = 1.20-2.97), and 2.01 (95% CI = 1.11-3.64), respectively; however, MDM2 SNP309 and C1797G did not show any significant difference between cases and controls. When TP53 and MDM2 polymorphisms were combined based on the numbers of variant risk alleles (i.e., G-allele of TP53 codon 72, G-allele of MDM2 SNP309, and G-allele of MDM2 C1797G), individuals with 3-5 variants had a 1.56-fold greater risk of PCa than those with 0-2 variants (95% CI = 1.07-2.26). Moreover, subjects with 0-2 variants had 33.3% positive p53 expression, whereas subjects with 3-5 variants had 23.3% p53 expression (P = 0.39). These findings suggest that TP53 and MDM2 polymorphisms play a role in PCa susceptibility in southern Chinese Han population.
Cancer genetics and cytogenetics 10/2010; 202(2):76-81. · 1.54 Impact Factor
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ABSTRACT: Vascular endothelial growth factor A (VEGF-A), a major driver of physiological and pathological angiogenesis, plays important roles in the etiology and metastasis of cancers. The +936C>T polymorphism in the 3'-untranslated region of the VEGFA gene has been implicated in cancer risk and is related to VEGF-A protein production; however, published data have been conflicting. To derive a more precise estimation of the relationship, a meta-analysis was performed of 13,293 cancer cases and 12,308 control subjects from 29 published case-control studies. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated to assess the association between +936C>T polymorphism and cancer risk. The meta-analysis indicated that individuals with the +936 T had increased risk of oral cancer (OR = 1.39, 95% CI = 1.03-1.88), although no association was found in the contrast of T versus C (OR = 1.00, 95% CI = 0.91-1.10) in the pooled analyses. This meta-analysis supports the idea that VEGFA + 936 T is associated with increased risk of oral cancer. To draw comprehensive and true conclusions, further prospective studies with larger numbers of participants worldwide are needed to examine associations between VEGFA + 936C>T polymorphism and cancer risk.
Cancer genetics and cytogenetics 04/2010; 198(1):7-14. · 1.54 Impact Factor
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Bin Xu,
Jinfeng Wang,
Na Tong,
YuanYuan Mi,
Zhichao Min, Jun Tao,
PengChao Li,
Gong Cheng,
JiuMing Li,
MeiLin Wang,
JiaLin Tang,
NingHong Song,
ZhengDong Zhang,
Wei Zhang,
HongFei Wu,
LiXin Hua,
NingHan Feng
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ABSTRACT: To explore the reported association of SNP marker rs10993994 with prostate cancer identified by two independent in two genome-wide association studies (GWAS) further, we performed a case-control study in southern Chinese Han population. Consequently, we detected the serum levels of MSMB expression with different genotypes in the cases and controls to characterize the functional consequences of rs10993994.
Two hundred fifty-one prostate cancer and 258 control subjects were included in the cancer association study and 90 serum samples were used to test the expression of the MSMB by Enzyme-linked immunosorbent assay (ELISA).
We found that the T allele displayed an increased prevalence of prostate cancer compared with the C allele (OR = 1.30, 95% CI = 1.01-1.67, P = 0.040). Moreover, the prostate cancer patients carrying CT/TT genotype had significantly decreased serum MSMB levels compared to those with CC genotype (16.32 +/- 3.98 microg/L vs. 19.33 +/- 4.27 microg/L, P = 0.022).
rs10993994 in MSMB promoter affects serum MSMB expression, contributes to the genetic predisposition to prostate cancer in southern Chinese Han population.
The Prostate 03/2010; 70(10):1146-52. · 3.48 Impact Factor
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Bin Xu,
Yuan-Yuan Mi,
Zhi-Chao Min,
Gong Cheng,
Na Tong, Jun Tao,
Peng-Chao Li,
Mei-Lin Wang,
Jia-Lin Tang,
Zheng-Dong Zhang,
Ning-Hong Song,
Wei Zhang,
Hong-Fei Wu,
Ning-Han Feng,
Li-Xin Hua
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ABSTRACT: Alterations in P53 and murine double minute 2 (MDM2) genes appear to be important in the development of many human tumors. We investigated the potential prognostic roles of p53 codon 72 and MDM2 309 and 1797 polymorphisms in prostate cancer after radical prostatectomy.
Fifty southern Chinese with prostate cancer undergoing radical prostatectomy were included in this study. All polymorphisms were detected by PCR-RFLP. Their prognosis on biochemical recurrence was assessed using Kaplan-Meier analysis and Cox regression model.
p53 codon 72 GG genotype was associated with increased biochemical recurrence compared with CG+CC genotypes and poorer PSA-free survival. It was also noted that GG genotype was an independent risk factor for biochemical recurrence after radical prostatectomy on multivariate analysis. No statistical difference was observed in MDM2 polymorphisms and prostate cancer prognosis.
Our data revealed that p53 codon 72 GG genotype carriers more frequently show biochemical recurrence than CG+CC genotypes carriers.
Urologia Internationalis 01/2010; 85(4):401-5. · 0.99 Impact Factor
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Bin Xu,
Ning-Han Feng,
Peng-Chao Li, Jun Tao,
Deyao Wu,
Zheng-Dong Zhang,
Na Tong,
Jin-Feng Wang,
Ning-Hong Song,
Wei Zhang,
Li-Xin Hua,
Hong-Fei Wu
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ABSTRACT: A G > C polymorphism (rs2910164) which is located in the sequence of miR-146a precursor, results in a change from a G:U pair to a C:U mismatch in its stem region. To explore whether rs2910164 plays any role in prostate cancer (CaP), we analyzed the association between miR-146a polymorphism and risk of CaP and the expression of miR-146a with different genotypes in CaP tissues in southern Chinese Han population.
Two hundred fifty-one CaP and 280 control subjects were included in the cancer association study, and 15 CaP tissue samples were used to test the expression of the miRNA precursors by real-time quantitative reverse transcription PCR.
We found that subjects carrying CC homozygotes had a 0.65-fold reduced risk (95% CI = 0.43-0.99) than those carrying GG/GC genotypes (P = 0.03), and the C allele displayed a lower prevalence of CaP compared with the G allele (OR = 0.73, 95% CI = 0.57-0.94, P = 0.01). Moreover, hsa-miR-146a quantification showed that homozygous carriers of the C-variant had significantly decreased miRNA levels compared to the carriers of the GG/GC genotype.
The natural genetic variation in pre-miR-146a affects the amount of mature miR-146a, contributes to the genetic predisposition to CaP.
The Prostate 11/2009; 70(5):467-72. · 3.48 Impact Factor
