Yiwei Lin

Zhejiang University, Hang-hsien, Zhejiang Sheng, China

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Publications (29)61.91 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Introduction: During the last decade, a bipolar plasmakinetic vaporization system with a novel button-like electrode has emerged and was described as a safe and effective option for the treatment of benign prostatic hyperplasia (BPH). Here, we present a modified technique named transurethral vapor enucleation of the prostate (TVEP). Materials and Methods: We provide a video that shows the main steps of this procedure. Vapo-enucleation of the prostate is performed by moving the button electrode circumferentially from the verumontanum toward the bladder neck, and the enucleated prostate tissue is retrieved by the morcellator. Three patients who were treated by TVEP in our institution between 2013 and 2014 were retrospectively evaluated to assess its feasibility. The postvoiding residual urine (PVRU) and maximum flow rate (Qmax) were measured preoperatively and 3 months postoperatively. Results: The mean operative time was 85 min. Nearly no vascular bleeding was observed during the operation. The average Qmax improved from 7.6 to 18.3 mL/s, and the PVRU decreased from 152 to 17 mL. Conclusions: TVEP seems to represent a promising endoscopic treatment alternative for BPH. No competing financial interests exist. Runtime of video: 7 mins 51 secs
    05/2015; DOI:10.1089/vid.2015.0010
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    ABSTRACT: MicroRNAs (miRNAs) are small, endogenous RNAs that play important gene-regulatory roles by binding to the imperfectly complementary sequences at the 3'-UTR of mRNAs and directing their gene expression. Here, we first discovered that miR-576-3p was down-regulated in human bladder cancer cell lines compared with the non-malignant cell line. To better characterize the role of miR-576-3p in bladder cancer cells, we over-expressed or down-regulated miR-576-3p in bladder cancer cells by transfecting with chemically synthesized mimic or inhibitor. The overexpression of miR-576-3p remarkably inhibited cell proliferation via G1-phase arrest, and decreased both mRNA and protein levels of cyclin D1 which played a key role in G1/S phase transition. The knock-down of miR-576-3p significantly promoted the proliferation of bladder cancer cells by accelerating the progression of cell cycle and increased the expression of cyclin D1. Moreover, the dual-luciferase reporter assays indicated that miR-576-3p could directly target cyclin D1 through binding its 3'-UTR. All the results demonstrated that miR-576-3p might be a novel suppressor of bladder cancer cell proliferation through targeting cyclin D1.
    Molecules and Cells 12/2014; 38(2). DOI:10.14348/molcells.2015.2146 · 2.24 Impact Factor
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    ABSTRACT: The mortality rate associated with prostate cancer is mainly due to metastases rather than primary organ‑confined disease. Decreasing the incidence of metastasis is important in treating prostate cancer. 4',5,7‑trihydroxyflavone (apigenin) has been demonstrated to be effective in inhibiting several types of cancer. The aim of this study was to investigate the effect and mechanism of apigenin on the movement of prostate cancer cells. In the present study, DU145 cells were treated with varying concentrations of apigenin for different time periods. Cell viability was evaluated using an MTT assay. Cell motility and invasiveness were assayed using wound healing assays and a Matrigel migration and invasion assay. Flow cytometric and western blot analyses were performed to examine the cell cycle and signaling pathways. The results demonstrated that apigenin suppressed the proliferation and inhibited the migration and invasive potential of the DU145 prostate cancer cells in a dose‑ and time‑dependent manner, which was associated with epithelial mesenchymal transition. These findings suggested that apigenin may be effective in treating human prostate cancer.
    Molecular Medicine Reports 10/2014; DOI:10.3892/mmr.2014.2801 · 1.48 Impact Factor
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    ABSTRACT: Background Increasing evidence has suggested that dysregulation of microRNAs (miRNAs) could contribute to human disease including cancer. Previous miRNA microarray analysis illustrated that miR-320c is down-regulated in various cancers. However, the roles of miR-320c in human bladder cancer have not been well elucidated. Therefore, this study was performed to investigate the biological functions and molecular mechanisms of miR-320c in human bladder cancer cell lines, discussing whether it could be a therapeutic biomarker of bladder cancer in the future.Methods Two human bladder cancer cell lines and samples from thirteen patients with bladder cancer were analyzed for the expression of miR-320c by quantitative RT-PCR. Over-expression of miR-320c was established by transfecting mimics into T24 and UM-UC-3. Cell proliferation and cell cycle were assessed by cell viability assay, flow cytometry and colony formation assay. Cell motility ability was evaluated by transwell assay. The target gene of miR-320c was determined by luciferase assay, quantitative RT-PCR and western blot. The regulation of cell cycle and mobility by miR-320c was analyzed by western blot.ResultsWe observed that miR-320c was down-regulated in human bladder cancer tissues and bladder cancer cell lines T24 and UM-UC-3. Over-expression of miR-320c could induce G1 phase arrest in UM-UC-3 and T24 cells, and subsequently inhibited cell growth. We also indentified miR-320c could impair UM-UC-3 and T24 cell motility. In addition, we identified CDK6, a cell cycle regulator, as a novel target of miR-320c. Moreover, we demonstrated miR-320c could induce bladder cancer cell cycle arrest and mobility via regulating CDK6. We also observed that inhibition of miR-320c or restoration of CDK6 in miR-320c-over-expressed bladder cancer cells partly reversed the suppressive effects of miR-320c.ConclusionsmiR-320c could inhibit the proliferation, migration and invasion of bladder cancer cells via regulating CDK6. Our study revealed that miR-320c could be a therapeutic biomarker of bladder cancer in the future.
    Journal of Experimental & Clinical Cancer Research 09/2014; 33(1):69. DOI:10.1186/PREACCEPT-1510670150130285 · 3.27 Impact Factor
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    ABSTRACT: Objective: We conducted a meta-analysis to quantitatively evaluate the correlation between alcohol consumption and the risk of urolithiasis by summarizing the results of published case-control and cohort studies and the potential dose-response association. Methods: A systematic literature search of articles up to February 2014 was conducted via PubMed, Web of Science, Cochrane Library, Scopus, EMBASE, the Chinese National Knowledge Infrastructure databases, and the references of the retrieved articles. Fixed- or random-effect models were used to summarize the estimates of odds ratio (OR) with 95% confidence interval (95% CI) for the highest versus the lowest consumption of alcohol. A dose-response meta-analysis was also conducted. Results: The pooled OR estimates indicated that alcohol consumption was associated with a decreased risk of urolithiasis (OR = 0.683, 95% CI 0.577-0.808). In addition, the dose-response meta-analysis indicated that the rate of urolithiasis decreased by 10% for a 10 g/day increase in alcohol intake (OR = 0.898, 95% CI 0.851-0.948). No evidence of publication bias was found by Begg's or Egger's test (p = 0.130, p = 0.130, respectively). Conclusion: Our meta-analysis indicated that alcohol intake is associated with a decreased risk of urolithiasis. © 2014 S. Karger AG, Basel.
    Urologia Internationalis 07/2014; 94(2). DOI:10.1159/000365358 · 1.15 Impact Factor
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    ABSTRACT: Hypereosinophilic syndrome (HES) is a rare disorder that is characterized by hypereosinophilia and organ damage, caused by the infiltration of eosinophils. In rare cases, the urinary bladder may also be involved. The current case report presented a 56-year-old male with gross hematuria and hypereosinophilia. The diagnosis of eosinophilic cystitis associated HES was established. Oral prednisone with a slow tapering regimen was administered as the primary treatment for the patient, which achieved partial hematological remission and complete relief of cystitis during a six-month follow-up period. Although eosinophilic cystitis is not commonly the primary manifestation of HES, eosinophilic cystitis should be taken into consideration following the onset of urinary symptoms in patients with HES.
    Experimental and therapeutic medicine 07/2014; 8(1):49-51. DOI:10.3892/etm.2014.1706 · 0.94 Impact Factor
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    ABSTRACT: Background Emerging evidence has suggested that dysregulation of miR-182-5p may contribute to tumor development and progression in several types of human cancers. However, its role in renal cell carcinoma (RCC) is still unknown. Methods Quantitative RT-PCR was used to quantify miR-182-5p expression in RCC clinical tissues. Bisulfite sequencing PCR was used for DNA methylation analysis. The CCK-8, colony formation, flow cytometry, and a xenograft model were performed. Immunohistochemistry was conducted using the peroxidase and DAB methods. A miR-182-5p target was determined by luciferase reporter assays, quantitative RT-PCR, and Western blotting. Results miR-182-5p is frequently down-regulated in human RCC tissues. Epigenetic modulation may be involved in the regulation of miR-182-5p expression. Enforced expression of miR-182-5p in RCC cells significantly inhibited the proliferation and tumorigenicity in vitro and in vivo. Additionally, overexpression of miR-182-5p induced G1-phase arrest via inhibition of AKT/FOXO3a signaling. Moreover, FLOT1 was confirmed as a target of miR-182-5p. Silencing FLOT1 by small interfering RNAs phenocopied the effects of miR-182-5p overexpression, whereas restoration of FLOT1 in miR-182-5p -overexpressed RCC cells partly reversed the suppressive effects of miR-182-5p. Conclusions These findings highlight an important role for miR-182-5p in the pathogenesis of RCC, and restoration of miR-182-5p could be considered as a potential therapeutic strategy for RCC therapy.
    Molecular Cancer 05/2014; 13(1):109. DOI:10.1186/1476-4598-13-109 · 5.40 Impact Factor
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    ABSTRACT: Arteriovesical fistulas are extremely rare. Only eleven cases were previously reported in the literature. They can occur iatrogenically, traumatically or spontaneously. We report an unusual case of a 62-year-old woman with arteriovesical fistula that developed fatal hematuria after transurethral electrocoagulation. Computed tomography (CT) and selective angiography revealed a pseudoaneurysm of the right superior vesical artery with arteriovesical fistula formation, which was managed by transarterial embolization. Contrast enhanced CT or CT angiography should be performed when a pulsatile hemorrhage is revealed during cystoscopy. Therapeutic vesical arterial embolization should be considered as a safe and effective procedure for arteriovesical fistulas. Transurethral electrocoagulation may cause severe hematuria for pulsatile bladder bleeding in patients with pelvic vascular malformation.
    BMC Urology 12/2013; 13(1):68. DOI:10.1186/1471-2490-13-68 · 1.94 Impact Factor
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    ABSTRACT: MicroRNAs (miRNAs) are non-protein-coding sequences that play a crucial role in tumorigenesis by negatively regulating gene expression. Here, we found that miR-490-5p is down-regulated in human bladder cancer tissue and cell lines compared to normal adjacent tissue and a non-malignant cell line. To better characterize the function of miR-490-5p in bladder cancer, we over-expressed miR-490-5p in bladder cancer cell lines with chemically synthesized mimics. Enforced expression of miR-490-5p in bladder cancer cells significantly inhibited the cell proliferation via G1-phase arrest. Further studies found the decreased c-Fos expression at both mRNA and protein levels and Luciferase reporter assays demonstrated that c-Fos is a direct target of miR-490-5p in bladder cancer. These findings indicate miR-490-5p to be a novel tumor suppressor of bladder cancer cell proliferation through targeting c-Fos.
    Biochemical and Biophysical Research Communications 11/2013; 441(4). DOI:10.1016/j.bbrc.2013.11.006 · 2.28 Impact Factor
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    ABSTRACT: Increasing evidence has suggested that dysregulation of certain microRNAs (miRNAs) may contribute to human disease including carcinogenesis and tumor metastasis in human. miR-124-3p is down-regulated in various cancers, and modulates proliferation and aggressiveness of cancer cells. However, the roles of miR-124-3p in human bladder cancer are elusive. Thus, this study was conducted to investigate the biological functions and its molecular mechanisms of miR-124-3p in human bladder cancer cell lines, discussing whether it has a potential to be a therapeutic biomarker of bladder cancer. Three human bladder cancer cell lines and samples from ten patients with bladder cancer were analyzed for the expression of miR-124-3p by quantitative RT--PCR. Exogenetic overexpression of miR-124-3p was established by transfecting mimics into T24, UM-UC-3 and J82 cells, after that cell proliferation and cell cycle were assessed by MTT assay, flow cytometry and Colony-forming assay. Cell motility and invasion ability were evaluated by wound healing assay and transwell assay. Tissue microarray, and immunohistochemistry with antibodies against ROCK1, MMP2 and MMP9 was performed using the peroxidase and DAB methods. The target gene of miR-124-3p was determined by luciferase assays, quantitative RT--PCR and western blot. The regulation of epithelial-to-mesenchymal transition by miR-124-3p was analyzed by western blot. miR-124-3p is frequently down-regulated in bladder cancer both in three bladder cancer cell lines, T24, UM-UC-3, J82 and clinical samples. Overexpression of miR-124-3p induced G1-phase arrest in T24, UM-UC-3 and J82 cell lines and suppressed cell growth in colony-forming assay. miR-124-3p significantly repressed the capability of migration and invasion of bladder cancer cells. In addition, ROCK1 was identified as a new target of miR-124-3p. ROCK1, MMP2, MMP9 were up-regulated in bladder cancer tissues. Furthermore, we demonstrated miR-124-3p could inhibit bladder cancer cell epithelial mesenchymal transfer, and regulated the expression of c-Met, MMP2, MMP9. miR-124-3p can repress the migration and invasion of bladder cancer cells via regulating ROCK1. Our data indicate that miR-124-3p could be a tumor suppressor and may have a potential to be a diagnostics or predictive biomarker in bladder cancer.
    Journal of Translational Medicine 11/2013; 11(1):276. DOI:10.1186/1479-5876-11-276 · 3.99 Impact Factor
  • 09/2013; 41(6). DOI:10.1007/s00240-013-0595-2
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    ABSTRACT: Previous cohort and case-control studies on the association between cruciferous vegetables consumption and risk of renal cell carcinoma have illustrated conflicting results so far. To demonstrate the potential association between them, a meta-analysis was performed. Eligible studies were retrieved via both computerized searches and review of references. The summary relative risks (RRs) with 95% confidence interval (CI) for the highest vs. the lowest consumption of cruciferous vegetables were calculated. Heterogeneity and publication bias were also evaluated. Stratified analyses were performed as well. Three cohort and 7 case-control studies were included. A significantly decreased risk with renal cell carcinoma was observed in overall cruciferous vegetables consumption group (RR = 0.73; 95% CI, 0.63-0.83) and subgroup of case-control studies (RR = 0.69; 95% CI, 0.60-0.78), but not in cohort studies (RR = 0.96; 95% CI, 0.71-1.21). No heterogeneity and publication bias were detected across studies. Our findings supported that cruciferous vegetables consumption was related to the decreased risk of renal cell carcinoma. Because of the limited number of studies, further well-designed prospective studies and researches need to be conducted to better clarify the protective effect of cruciferous vegetables on renal cell carcinoma and potential mechanism.
    Nutrition and Cancer 07/2013; 65(5):668-76. DOI:10.1080/01635581.2013.795980 · 2.47 Impact Factor
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    ABSTRACT: It is increasingly clear that microRNAs play a crucial role in tumorigenesis. Recently, emerging evidence suggested that miR-26a is aberrantly expressed in tumor tissues. In our study, frequent down-regulation of miR-26a was observed in 10 human bladder cancer tissues. Forced expression of miR-26a in the bladder cancer cell line T24 inhibited cell proliferation and impaired cell motility. HMGA1, a gene that modulates cell cycle transition and cell motility, was verified as a novel target of miR-26a in bladder cancer. These findings indicate an important role for miR-26a in the molecular etiology of bladder cancer and implicate the potential application of miR-26a in bladder cancer therapy.
    FEBS letters 06/2013; 587(15). DOI:10.1016/j.febslet.2013.06.021 · 3.34 Impact Factor
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    ABSTRACT: BACKGROUND: Apigenin (4',5,7-trihydroxyflavone) was recently shown effective in inhibiting several cancers. The aim of this study was to investigate the effect and mechanism of apigenin in the human bladder cancer cell line T24 for the first time. METHODS: T24 cells were treated with varying concentrations and time of apigenin. Cell viability was evaluated by MTT assay. Cell motility and invasiveness were assayed by Matrigel migration and invasion assay. Flow cytometry and western blot analysis were used to detect cell apoptosis, cell cycle and signaling pathway. RESULTS: The results demonstrated that apigenin suppressed proliferation and inhibited the migration and invasion potential of T24 bladder cancer cells in a dose- and time-dependent manner, which was associated with induced G2/M Phase cell cycle arrest and apoptosis. The mechanism of action is like to involve PI3K/Akt pathway and Bcl-2 family proteins. Apigenin increased caspase-3 activity and PARP cleavage, indicating that apigenin induced apoptosis in a caspase-dependent way. CONCLUSIONS: These findings suggest that apigenin may be an effective way for treating human bladder cancer.
    Cancer Cell International 06/2013; 13(1):54. DOI:10.1186/1475-2867-13-54 · 1.99 Impact Factor
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    ABSTRACT: There is increasing evidence suggesting that dysregulation of certain microRNAs (miRNAs) may contribute to tumor progression and metastasis. Previous studies have shown that miR-409-3p is dysregulated in some malignancies, but its role in bladder cancer is still unknown. Here, we find that miR-409-3p is down-regulated in human bladder cancer tissues and cell lines. Enforced expression of miR-409-3p in bladder cancer cells significantly reduced their migration and invasion without affecting cell viability. Bioinformatics analysis identified the pro-metastatic gene c-Met as a potential miR-409-3p target. Further studies indicated that miR-409-3p suppressed the expression of c-Met by binding to its 3'-untranslated region. Silencing of c-Met by small interfering RNAs phenocopied the effects of miR-409-3p overexpression, whereas restoration of c-Met in bladder cancer cells bladder cancer cells overexpressing miR-409-3p, partially reversed the suppressive effects of miR-409-3p. We further showed that MMP2 and MMP9 may be downstream effector proteins of miR-409-3p. These findings indicate that miR-409-3p could be a potential tumor suppressor in bladder cancer.
    Moleculer Cells 05/2013; 36(1). DOI:10.1007/s10059-013-0044-7 · 2.24 Impact Factor
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    ABSTRACT: microRNAs (miRNAs), small non-coding RNAs, have emerged as key regulators of a large number of genes. The present study aimed to explore novel biological functions of miR-330 in the human prostate cancer cell lines DU145 and PC3. We confirmed that miR-330 was downregulated and inversely correlated with specificity protein 1 (Sp1) expression. Overexpression of miR-330 by transfection of a chemically synthesized miR-330 mimic induced a reduction in expression levels of the Sp1 protein, accompanied by significant suppression of cellular migration and invasion capability. In addition, the Sp1-knockdown experiments presented similar phenomena. Finally, the luciferase reporter assay validated Sp1 as the direct target of miR-330. These findings indicate that miR-330 acts as an anti-metastatic miRNA in prostate cancer.
    Oncology Reports 05/2013; 30(1). DOI:10.3892/or.2013.2452 · 2.19 Impact Factor
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    ABSTRACT: MicroRNAs (miRNAs) are small non-coding RNAs that play regulatory roles by repressing translation or cleaving RNA transcripts. Here, we report that the expression of microRNA-101 (miR-101) is down-regulated in human bladder cancer tissue versus normal adjacent tissue. To better characterize the role of miR-101 in bladder cancer, we conducted a gain-of-function analysis by transfecting the bladder cancer cell line T24 with chemically synthesized miR-101 mimics. We found that miR-101 directly targets c-Met via its 3'-UTR. Specifically, forced expression of miR-101 decreased c-Met expression at both mRNA and protein levels, consequently inhibiting T24 cell migration and invasion in a c-Met-dependent manner. In conclusion, we have shown miR-101 to be a novel suppressor of T24 cell migration and invasion through its negative regulation of c-Met.
    Biochemical and Biophysical Research Communications 04/2013; DOI:10.1016/j.bbrc.2013.04.042 · 2.28 Impact Factor
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    ABSTRACT: BACKGROUND: The XRCC1 polymorphisms have been implicated in bladder cancer risk, but individually published studies show inconsistent results. The aim of our study was to clarify the effects of XRCC1 variants on bladder cancer risk. METHODS: A systematic literature search up to September 13, 2012 was carried out in PubMed, EMBASE and Wanfang databases, and the references of retrieved articles were screened. Crude odds ratios with 95% confidence intervals were used to assess the associations between XRCC1 Arg194Trp and Arg399Gln polymorphisms and bladder cancer risk. Heterogeneity and publication bias were also evaluated. RESULTS: A total of 14 and 18 studies were eligible for meta-analyses of Arg194Trp and Arg399Gln, respectively. Regrouping was adopted in accordance with the most probable appropriate genetic models. No obvious heterogeneity between studies was found. For overall bladder cancer, the pooled odds ratios for Arg194Trp and Arg399Gln were 1.69 (95% confidence interval: 1.25 to 2.28; P = 0.001) and 1.10 (95% confidence interval: 1.03 to 1.19; P = 0.008), respectively. After excluding the studies that were not in Hardy--Weinberg equilibrium, the estimated pooled odds ratio still did not change at all. CONCLUSIONS: The meta-analysis results suggest that XRCC1 Arg194Trp and Arg399Gln polymorphisms may be associated with elevated bladder cancer risk.
    World Journal of Surgical Oncology 03/2013; 11(1):58. DOI:10.1186/1477-7819-11-58 · 1.20 Impact Factor
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    ABSTRACT: Diabetes is associated with increased risk of cancer at several sites, but its association with risk of bladder cancer is still controversial. We examined this association by conducting a systematic review and meta-analysis of cohort studies. Studies were identified by searching PubMed, EMBASE, Scopus, Web of Science, Cochrane register, and Chinese National Knowledge Infrastructure (CNKI) databases through April 29, 2012. Summary relative risks (SRRs) with their corresponding 95% confidence intervals (CIs) were calculated using a random-effects model. A total of fifteen cohort studies were included in this meta-analysis. Analysis of all studies showed that diabetes was associated with a borderline statistically significant increased risk of bladder cancer (RR 1.11, 95% CI 1.00-1.23; p<0.001 for heterogeneity; I = 84%). When restricting the analysis to studies that had adjusted for cigarette smoking (n = 6) or more than three confounders (n = 7), the RRs were 1.32 (95% CI 1.18-1.49) and 1.20 (95% CI 1.02-1.42), respectively. There was no significant publication bias (p = 0.62 for Egger's regression asymmetry test). Our findings support that diabetes was associated with an increased risk of bladder cancer. More future studies are warranted to get a better understanding of the association and to provide convincing evidence for clinical practice in bladder cancer prevention.
    PLoS ONE 03/2013; 8(3):e58079. DOI:10.1371/journal.pone.0058079 · 3.53 Impact Factor
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    ABSTRACT: Plasminogen activator inhibitor-1 (PAI-1), belonging to the urokinase plasminogen activation (uPA) system, is involved in cancer development and progression. The PAI-1 promoter 4G/5G polymorphism was shown to contribute to genetic susceptibility to cancer, although the results were inconsistent. To assess this relationship more precisely, a meta-analysis was performed. The electronic databases PubMed, Scopus, Web of Science and Chinese National Knowledge Infrastructure (CNKI) were searched; data were extracted and analyzed independently by two reviewers. Ultimately, 21 eligible case-control studies with a total of 8,415 cancer cases and 9,208 controls were included. The overall odds ratio (OR) with its 95% confidence interval (CI) showed a statistically significant association between the PAI-1 promoter 4G/5G polymorphism and cancer risk (4G/4G vs. 5G/5G: OR=1.25, 95% CI=1.07-1.47, P(heterogeneity)=0.001; 4G/4G vs. 4G/5G+5G/5G: OR=1.10, 95% CI=1.03-1.17, P(heterogeneity)=0.194; 4G/4G+4G/5G vs. 5G/5G: OR=1.17, 95% CI=1.01-1.35, P(heterogeneity)=0.041). In further subgroup analyses, the increased risk of cancer was observed in a subgroup of Caucasians with regards to endometrial cancer. Our meta-analysis suggests that the PAI-1 4G/5G polymorphism most likely contributes to susceptibility to cancer, particularly in Caucasians. Furthermore, the 4G allele may be associated with an increased risk of endometrial cancer.
    Experimental and therapeutic medicine 12/2012; 4(6):1127-1133. DOI:10.3892/etm.2012.734 · 0.94 Impact Factor

Publication Stats

153 Citations
61.91 Total Impact Points

Institutions

  • 2010–2014
    • Zhejiang University
      • School of Medicine
      Hang-hsien, Zhejiang Sheng, China
  • 2013
    • Affiliated Urology Specialists
      Peoria, Illinois, United States
  • 2012
    • Zhejiang Medical University
      • Department of Urology
      Hang-hsien, Zhejiang Sheng, China