Daiming Fan

Fourth Military Medical University, Xi’an, Liaoning, China

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Publications (446)1845.94 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Until now, no data on the routine screening for thrombotic risk factors in Chinese nonmalignant and noncirrhotic patients with portal vein thrombosis (PVT) have been reported. A total of 141 nonmalignant and noncirrhotic patients with PVT who underwent screening tests for thrombotic risk factors between September 2009 and August 2012 were included in this study. The JAK2 V617F mutation was found in 35 of the 141 patients tested. Neither the JAK2 exon 12 mutation nor the MPL W515 L/K mutation was found in any of the 50 patients tested. Overt myeloproliferative neoplasms (MPNs) were diagnosed in 13 patients (polycythemia vera, n=1; essential thrombocythemia, n=9; idiopathic myelofibrosis, n=3). Latent MPNs were considered in 23 patients with the JAK2 V617F mutation but without any significant abnormalities, as determined through regular blood tests. Anticardiolipin IgG antibodies were positive in none of the 136 patients tested. Paroxysmal nocturnal hemoglobinuria was not found in any of the 141 patients tested. Neither the factor V G1691A mutation nor the factor II G20210A mutation was found in any of the 72 patients tested. The C677T mutation in 5,10-methylenetetrahydrofolate reductase (MTHFR) was found in 29 of the 38 patients tested. Hyperhomocysteinemia was detected in eight of the 39 patients tested. MPNs are an important thrombotic risk factor in Chinese patients with PVT. However, the extreme rarity of paroxysmal nocturnal hemoglobinuria, anticardiolipin IgG antibodies, and factor V G1691A and factor II G20210A mutations has precluded any support for the implementation of routine screening for these thrombotic factors in such patients. Additional case-control studies should confirm the role of the MTHFR C677T mutation and hyperhomocysteinemia in the pathogenesis of PVT.
    European journal of gastroenterology & hepatology. 01/2015; 27(1):77-83.
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    ABSTRACT: Loss of cell-cell adhesion is important for the development of cancer invasion and metastasis. Vinculin, a key adhesion-related protein, can affect metastasis and prognosis in several tumours. Here, we determined the biological roles of vinculin in the metastasis of colorectal cancer (CRC) and evaluated its clinical significance as a potential disease biomarker. The expression level of vinculin in CRC cell lines and tissues was measured using Real-Time PCR and western blotting. Moreover, vinculin function was analysed using Transwell assays and in vivo metastasis assays in gain- and loss-of-function experiments. Furthermore, the impact of vinculin together with membrane-bound beta-catenin on the prognosis of 228 CRC patients was investigated by immunohistochemistry. Additionally, the expression of epithelial-mesenchymal transition (EMT) indicators was verified by immunohistochemistry in CRC tissues obtained from these patients.Result: Vinculin expression was found to be significantly downregulated in highly metastatic CRC cell lines and metastatic tissues. Both in vitro and in vivo experiments showed that vinculin suppressed invasion, migration and metastasis in CRC cells and that this suppression could be attenuated by silencing beta-catenin. Moreover, the expression of vinculin and membrane-bound beta-catenin were positively correlated in CRC tissues, and lack of vinculin expression emerged as an independent prognostic factor in patients with CRC. Finally, the loss of vinculin and membrane-bound beta-catenin was associated with node metastasis, organ metastasis and expression of EMT indicators. Our results suggest that vinculin may play specific roles in the EMT and metastasis of CRC and that loss of vinculin could be used as a prognostic factor for CRC.
    Molecular cancer. 12/2014; 13(1):263.
  • Xiangqiang Liu, Daiming Fan
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    ABSTRACT: The epithelial-mesenchymal transition (EMT) is a highly conserved cellular process that transforms epithelial cells into mesenchymal cells; EMT is involved in normal embryogenesis and tissue repair and contributes to tumor progression, including tumor metastasis, therapy resistance and disease recurrence. Cancer stem cells (CSCs) represent a fraction of undifferentiated cancer cells that exhibit stem cell-like features. They have the ability to self-renew and can seed new tumors. Thus, CSCs might represent the cellular resource that causes metastases and accounts for therapy resistance. Recent studies have highlighted a link between EMT and CSC formation. EMT is relevant to the acquisition and maintenance of stem cell-like characteristics and is sufficient to endow differentiated normal and cancer cells with stem cell properties. Moreover, CSCs often exhibit EMT properties. This reciprocal relationship between EMT and CSCs might have many implications in tumor progression. In this paper, we review current studies related to EMT and CSCs in tumor progression and therapeutic resistance, with a special focus on the common characteristics and links between these processes, and explore the importance of these links in the development of improved antitumor therapies.
    Current pharmaceutical design. 12/2014;
  • Xingshun Qi, Xiaozhong Guo, Daiming Fan
    Hepatology 12/2014; · 12.00 Impact Factor
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    ABSTRACT: The risk of venous thromboembolism (VTE) may be increased in patients with liver diseases. A systematic review and meta-analysis were conducted to analyze the epidemiology of VTE in such patients. All relevant studies were searched via the PubMed, EMBASE, and Cochrane Library databases. The incidence and prevalence of VTE were pooled using random-effect models. Subgroup analyses were conducted according to the type of VTE [deep vein thrombosis (DVT), pulmonary embolism (PE)], type of liver disease (liver cirrhosis alone/unclassified liver diseases or non-cirrhotics), region in which the study was performed (USA/Europe/Asia), number of total observed patients with liver diseases (>1,000/<1,000 patients), study quality (high/low), and methods for identifying the cases (ICD codes/clinical charts). Of 4,843 papers initially identified, 20 were included. The incidence of VTE varied from 0.33 to 6.32 % in 14 studies with a pooled value of 1 % (95 % confidence interval (CI) 0.7-1.3 %). The pooled incidence of DVT and PE was 0.6 % (95 % CI 0.4-0.8 %) and 0.28 % (95 % CI 0.13-0.49 %), respectively. The prevalence of VTE varied from 0.6 to 4.69 % in six studies with a pooled value of 1.0 % (95 % CI 0.7-1.2 %). The pooled prevalence of DVT and PE was 0.7 % (95 % CI 0.6-0.9 %) and 0.36 % (95 % CI 0.13-0.7 %), respectively. The heterogeneity was statistically significant in the main and subgroup meta-analyses. In conclusion, about 1 % of patients with liver diseases develop or are diagnosed with VTE during their hospitalizations. However, the epidemiological data are very heterogeneous among studies.
    Internal and Emergency Medicine 12/2014; · 2.35 Impact Factor
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    ABSTRACT: Hypoxia has been implicated as a crucial microenvironmental factor that induces cancer metastasis. We previously reported that hypoxia could promote gastric cancer (GC) metastasis, but the underlying mechanisms are not clear. Long noncoding RNAs (lncRNAs) have recently emerged as important regulators of carcinogenesis that act on multiple pathways. However, whether lncRNAs are involved in hypoxia-induced GC metastasis remains unknown. In this study, we investigated the differentially expressed lncRNAs resulting from hypoxia-induced GC and normoxia conditions using microarrays and validated our results through real-time quantitative polymerase chain reaction. We found an lncRNA, AK058003, that is upregulated by hypoxia. AK058003 is frequently upregulated in GC samples and promotes GC migration and invasion in vivo and in vitro. Furthermore, AK058003 can mediate the metastasis of hypoxia-induced GC cells. Next, we identified γ-synuclein (SNCG), which is a metastasis-related gene regulated by AK058003. In addition, we found that the expression of SNCG is positively correlated with that of AK058003 in the clinical GC samples used in our study. Furthermore, we found that the SNCG gene CpG island methylation was significantly increased in GC cells depleted of AK058003. Intriguingly, SNCG expression is also increased by hypoxia, and SNCG upregulation by AK058003 mediates hypoxia-induced GC cell metastasis. These results advance our understanding of the role of lncRNA-AK058003 as a regulator of hypoxia signaling, and this newly identified hypoxia/lncRNA-AK058003/SNCG pathway may help in the development of new therapeutics. Copyright © 2014 Neoplasia Press, Inc. Published by Elsevier Inc. All rights reserved.
    Neoplasia (New York, N.Y.) 12/2014; 16(12):1094-106. · 5.48 Impact Factor
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    ABSTRACT: Mesenchymal stem cells (MSCs) have been shown to integrate into the tumor stroma; however, the precise mechanisms of this process are still elusive. In this study, the EMT phenotype and the enhanced metastatic ability of tumor cells were observed using transwell and trans-endothelial migration assays, respectively, as well as by using electron and laser confocal microscopy. Critical genes were screened and validated using gene arrays and clinical samples, and the changes at the protein level were examined both in vitro and in vivo. Cancer cells acquired an “activated” carcinoma-associated fibroblasts (CAFs) phenotype after being in close contact with MSCs and enhancing tumor metastasis and growth in vivo. Paracrine signals also induced EMT and promoted transwell and trans-endothelial migration, the changes were dependent on β-catenin, MMP-16, snail and twist. Notably, the higher expression levels of β-catenin and MMP-16 were correlated with tumor invasion and distant organ and lymph node metastases in intestinal type gastric cancer. MSCs within the tumor niche significantly facilitated tumor growth and metastasis by paracrine cues and close physical connection. This occurred partly through snail, twist and its downstream targets, specifically β-catenin/MMP-16. This article is protected by copyright. All rights reserved
    Journal of Cellular Biochemistry 11/2014; · 3.06 Impact Factor
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    ABSTRACT: Uncontrolled proliferation is a key characteristic of gastric carcinogenesis and the precise mechanisms underlying the altered proliferation behaviors of GC cells have not been clearly elucidated. miRNAs has been suggested to play a crucial role in the pathogenesis and development of various cancers. In the present study, we employed an impedance-based real-time cell electronic sensing (RT-CES) system to detect the effects of ectopically expressed miRNAs on GC cell proliferation.
    Journal of Cancer Research and Clinical Oncology 10/2014; · 2.91 Impact Factor
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    ABSTRACT: To investigate and compare the efficacy and safety of percutaneous transhepatic biliary stenting (PTBS) using a one- or two-stage procedure and determine the predictive factors for the efficacious treatment of malignant hilar obstruction (MHO).
    Cardiovascular and interventional radiology. 10/2014;
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    ABSTRACT: Recent studies have reported that hyper-methylation in the promoter region of miRNAs could silence the expression of tumor suppressive miRNAs and might play significant roles in the process of tumor development. However, the potential mechanisms regarding how methylation of miRNA CpG Island could regulate cancer cell chemo-resistance have not yet been studied. Using microarray and BSP (Bisulfate Sequencing PCR) assays, we found that compared with the parent SGC7901/VCR cells, expression of miR-129-5p was restored in SGC7901/VCR gastric cancer multi-drug resistant cell line treated by de-methylation reagent (5-AZA-dC). Using gain or loss of function assays, we found the over-expressed miR-129-5p reduced the chemo-resistance of SGC7901/VCR and SGC7901/ADR cells, while down-regulation of miR-129-5p had an opposite effect. Furthermore, three members of multi-drug resistance (MDR) related ABC transporters (ABCB1, ABCC5 and ABCG1) were found to be direct targets of miR-129-5p using bioinformatics analysis and report gene assays. The present study indicated that hyper-methylation of miR-129-5p CpG island might play important roles in the development of gastric cancer chemo-resistance by targeting MDR related ABC transporters and might be used as a potential therapeutic target in preventing the chemo-resistance of gastric cancer.
    Oncotarget 10/2014; · 6.64 Impact Factor
  • Xingshun Qi, Xiaozhong Guo, Daiming Fan
    Cardiovascular and interventional radiology. 10/2014;
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    Xingshun Qi, Zhiping Yang, Daiming Fan
    Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology Association. 09/2014; 20(5):265-266.
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    ABSTRACT: An increasing body of evidence indicates that miRNAs have a critical role in carcinogenesis and cancer progression; however, the role of miRNAs in the tumorigenesis of adencarcinoma of gastric esophageal junction (AGEJ) remains largely unclear.
    BMC Cancer 08/2014; 14(1):633. · 3.33 Impact Factor
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    ABSTRACT: Acute variceal bleeding is the most common lethal complication of liver cirrhosis. A meta-analysis was conducted to compare the outcomes of transjugular intrahepatic portosystemic shunt (TIPS) to those of medical/endoscopic therapy for acute variceal bleeding in cirrhotic patients.
    Journal of clinical gastroenterology. 08/2014;
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    ABSTRACT: AbstactBackground and AimThe gut microbiota plays a pivotal role in the intestinal diseases. Fecal microbiota transplantation (FMT) might be a rescue therapy for refractory inflammatory bowel disease. This study aimed to evaluate the safety, feasibility and efficacy of FMT through mid-gut for refractory Crohn's disease (CD).Methods We established standardized laboratory protocol and clinical work flow for FMT. Only refractory CD patients with Harvey-Bradshaw Index (HBI) score ≥ 7 were enrolled for this study. All included patients were treated with single FMT through mid-gut and assessed during follow-up.ResultsMetagenomics analysis showed a high concordance between feces sample and purified fecal microbiota from same donors. Standardized fecal microbiota preparation and clinical flow significantly simplified the practical aspects of FMT. Totally 30 patients were qualified for the present analysis. The rate of clinical improvement and remission based on clinical activity at the first month was 86.7 % (26/30) and 76.7 % (23/30) respectively, which was higher than other assessment points within 15-month follow-up. Patients’ body weight increased after FMT, and the lipid profile improved as well. FMT also showed a fast and continuous significant effect in relieving the sustaining abdominal pain associated with sustaining CD.Conclusions This is a pilot study with the largest sample of patients with refractory CD underwent single FMT. The results demonstrated that FMT through mid-gut might be a safe, feasible, and efficient rescue therapy for refractory CD.
    Journal of Gastroenterology and Hepatology 08/2014; · 3.33 Impact Factor
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    ABSTRACT: Dysregulation of transcription factors (TFs) is associated with tumor progression, but little is known about TF expression patterns in the context of gastric cancer (GC) metastasis. Using array-based profile analysis, we found that 22 TFs showed differential activities between GC cell lines with low- and high-metastatic potential. Of this group of TFs, serum response factor (SRF) was significantly upregulated in metastatic GC cells. SRF expression was frequently elevated in a panel of metastatic GC cells and tissues, and high-level expression of SRF was significantly associated with a more aggressive phenotype and poor prognosis in patients with GC. In GC cell lines, overexpression of SRF potently promoted cell migration and invasion in vitro as well as the formation of intrahepatic and pulmonary metastases in vivo, whereas loss of SRF inhibited GC cell invasion and metastasis. We also performed a microRNA microarray to screen for transcriptional targets of SRF and found that SRF transactivates miR-199a-5p and miR-199a-3p by directly binding to their promoters. We further determined that overexpression of miR-199a-5p, but not miR-199a-3p, increased GC cell invasion and metastasis. In contrast, inhibition of miR-199a-5p impaired the metastatic potential of GC cells in vitro and in vivo, and E-cadherin was identified as a direct and functional target of miR-199a-5p in GC cells. Specifically, our results showed that SRF promotes GC metastasis and the epithelial to mesenchymal transition (EMT) though miR-199a-5p-mediated downregulation of E-cadherin. The present study thus provides insight into the specific biological behavior of SRF in GC metastasis. As increased activity of the SRF/miR-199a-5p/E-cadherin pathway appears to promote GC cell EMT and metastasis, these regulators may therefore be developed as therapeutic targets or biomarkers for GC progression.Cell Death and Differentiation advance online publication, 1 August 2014; doi:10.1038/cdd.2014.109.
    Cell death and differentiation. 08/2014;
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    ABSTRACT: Context.-The expression of membrane-bound complement regulatory proteins (mCRPs) that inhibit the complement system in normal tissues is essential for self-protection against an autologous immune reaction. However, the expression patterns of mCRPs, including CD46, CD55, and CD59, are inconsistent in different types of cancer cells. Objectives.-To determine whether CD46, CD55, and CD59 are differentially expressed in neoplastic and adjacent normal colon tissues and to assess their clinical significance. Design.-Immunohistochemistry was performed on tissue microarrays of cancerous and adjacent normal colon tissues. Results.-The expression levels of CD46, CD55, and CD59 were significantly higher in colon cancer tissues compared with the normal adjacent colon tissues. We found that the expression levels of CD55 and CD59 correlated with the grade of differentiation in colon cancers. In addition, the expression of CD55 and CD59 was greater in stage III and stage IV colon cancers than in stage I and stage II cancers according to staging by the TNM classification. Conclusions.-CD46, CD55, and CD59 are up-regulated in colon cancer. Specifically, CD55 and CD59 are of clinical relevance to differentiation and TNM staging of colon cancer. These data suggest that CD46, CD55, and CD59 have the potential to be used for molecular staging diagnoses and for colon cancer therapies.
    Archives of pathology & laboratory medicine 07/2014; 138(7):910-919. · 2.78 Impact Factor
  • Lina Cui, Yongquan Shi, Ying Han, Daiming Fan
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    ABSTRACT: Unbalanced immune cell populations or immune cell infiltration of the liver can disrupt the immune-privileged state of the liver, resulting in liver injury or fibrosis. Therefore, the treatment for liver diseases involves not only hepatic regeneration but also immunological regulation. Recent studies demonstrated that stem cells, especially mesenchymal stem cells, have the capacity for not only hepatic differentiation but also immunomodulation. In this respect, stem cell therapy could be a realistic aim for liver diseases by modulating the liver regenerative processes and down-regulating immune-mediated liver damage. In this review, we discuss in detail the importance of immune cells in liver injury and repair; the mechanism by which stem cells demonstrate an immune-tolerant phenotype that can be used for allogeneic transplantation; the effect of stem cell transplantation on immune-mediated diseases, especially liver diseases; and the mechanism by which stem cells improve the hepatic microenvironment.
    Expert Review of Clinical Immunology 06/2014; · 2.89 Impact Factor
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    ABSTRACT: Multidrug resistance (MDR) is the most common cause of chemotherapy failure in gastric cancer (GC) treatment; however, the underlying molecular mechanisms remain elusive. Long non-coding RNAs (lncRNAs) can be involved in carcinogenesis, but the effects of lncRNAs on MDR are poorly understood. We show herein that the lncRNA, MRUL (MDR-related and up-regulated lncRNA), located 400 kb downstream of ABCB1 (ATP-binding cassette, sub-family B, member 1), was significantly up-regulated in two multidrug-resistant GC cell sublines, SGC7901/ADR and SGC7901/VCR. Furthermore, the relative expression levels of MRUL in GC tissues were negatively correlated with in vitro growth inhibition rates of GC specimens treated with chemotherapy drugs and indicated a poor prognosis for GC patients. MRUL knockdown in SGC7901/ADR and SGC7901/VCR cells led to increased rates of apoptosis, increased accumulation, and reduced Adriamycin release in the presence of Adriamycin or vincristine. Moreover, MRUL depletion reduced ABCB1 mRNA levels in a dose- and time-dependent manner. Heterologous luciferase reporter assays demonstrated that MRUL might positively affect ABCB1 expression in an orientation- and position-independent manner. Our findings indicate that MRUL plays a positive role in the regulation of ABCB1 expression and is a potential target to reverse the MDR phenotype of GC MDR cell sublines.
    Molecular and cellular biology. 06/2014;
  • X Qi, S Hu, W Hou, J Jia, G Han, D Fan
    Journal of Gastroenterology and Hepatology 06/2014; 29(6). · 3.33 Impact Factor

Publication Stats

5k Citations
1,845.94 Total Impact Points


  • 2000–2014
    • Fourth Military Medical University
      • • State Key Laboratory of Cancer Biology
      • • Department of Gastroenterology
      Xi’an, Liaoning, China
    • Virginia Commonwealth University
      • School of Medicine
      Richmond, VA, United States
  • 2009–2011
    • State Key Laboratory of Medical Genetics of China
      Ch’ang-sha-shih, Hunan, China
  • 1998–2010
    • Xi'an Jiaotong University
      • • School of Science
      • • Department of Gastroenterology
      Xi’an, Shaanxi Sheng, China
  • 2008
    • Logistical College of Chinese People's Armed Police Force
      T’ien-ching-shih, Tianjin Shi, China
  • 2004
    • Huazhong University of Science and Technology
      Wu-han-shih, Hubei, China
  • 2002
    • General Hospital of Jinan Military Region
      Chi-nan-shih, Shandong Sheng, China
  • 2001–2002
    • Southern Medical University
      Shengcheng, Guangdong, China
  • 1997–2001
    • Emory University
      • Department of Internal Medicine
      Atlanta, GA, United States