Daiming Fan

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

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Publications (490)2144.8 Total impact

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    Yong Lv · Daiming Fan
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    ABSTRACT: The role of transjugular intrahepatic portosystemic shunt (TIPS) for the secondary prophylaxis of variceal bleeding in cirrhotic patients with portal vein thrombosis (PVT) remains obscure. This prospective cohort study aimed to assess the risk factors associated with TIPS technical success, outcome, and prognosis in cirrhotic patients with PVT and a history of variceal bleeding. Between May 2009 and April 2011, 51 cirrhotic patients with PVT who attempted TIPS procedures for the prevention of variceal rebleeding were enrolled. TIPS success rate was 84% (43/51). An increased degree of thrombosis within the portal trunk and portal vein branches was inversely associated with TIPS success. Median follow-up time was 40.07 months (range: 0.02-56.87). The cumulative risk of rebleeding was significantly different between TIPS success and failure group (p=0.002). The univariate analysis also demonstrated that TIPS failure was the only significant predictor associated with rebleeding (hazard ratio [HR]=4.174, 95% confidence interval [CI]: 1.558-11.186). In TIPS success group, the cumulative rates free of shunt dysfunction at the 6(th) and 12(th) month were 79% and 76%, respectively. Absence of total superior mesenteric vein (SMV) thrombosis was the only independent predictor (HR=0.189, 95%CI: 0.047-0.755). In TIPS success group, the 1- and 3-year cumulative survival rates were 77% and 62%, respectively. Albumin level was the only independent predictor (HR=0.877, 95% CI: 0.779-0.986). Successful TIPS insertions could effectively prevent from rebleeding in cirrhotic patients with PVT and variceal bleeding. Degree of PVT and SMV thrombosis was associated with TIPS failure and shunt dysfunction, respectively. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    Liver international: official journal of the International Association for the Study of the Liver 08/2015; DOI:10.1111/liv.12929 · 4.41 Impact Factor
  • Liu Hong · Yu Han · Jinqiang Liu · Daiming Fan
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    ABSTRACT: Introduction: The treatment effects of advanced solid cancer are unsatisfactory, and novel therapeutic approaches are much needed. Keratinocyte growth factor receptor (KGFR) is a receptor tyrosine kinase that is primarily localized on epithelial cells. KGFR may play important roles in epithelial cell proliferation and differentiation, epithelial wound repair, embryonic development, immunity, tumor formation and development.Areas covered: This review summarizes the expression, function and mechanism of KGFR in solid cancer, and analyzes its value for the cancer therapy. Furthermore, this study discusses the limitations of KGFR-based therapy, and envisages future developments in the clinical applications of KGFR.Expert opinion: KGFR may function as an ideal therapeutic target for solid cancer. Continued basic investigation of KGFR-mediated pathways will push insight into the novel strategies of target therapy. More in vivo studies and clinical trials should be performed to promote the translational bridging of the latest research into clinical application.
    Expert Opinion on Therapeutic Targets 07/2015; DOI:10.1517/14728222.2015.1062474 · 4.90 Impact Factor
  • Liu Hong · Yu Han · Hongwei Zhang · Daiming Fan
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    ABSTRACT: Esophageal cancer (EC) remains a leading cause of cancer-related death in Asian countries. Due to the biology of EC, including aggressive local invasion, early metastasis and drug resistance, EC has a low survival rate. Therefore, molecular markers for prognosis judgment are urgently required so as to identify subgroups of patients that will benefit from more aggressive therapeutic interventions. So far, many genes and miRNAs, such as VEGF, cyclin D1, and miR-21, have been shown to be valuable when predicting the prognosis of EC. Some circulating molecules, including miR-200c, miR-1246, miR-31, have been identified as the independent risk factors for poor survival. However, the function and mechanism of these molecules in EC remains unclear. More clinical studies should be performed to promote the clinical use of prognosis-related markers in the management of EC.
    Expert review of gastroenterology & hepatology 06/2015; 9(7):1-3. DOI:10.1586/17474124.2015.1041507 · 2.55 Impact Factor
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    ABSTRACT: BACKGROUND&AIMS: Inflammation regulated by interleukin-8 (IL8) promotes metastasis of hepatocellular carcinoma (HCC). The transcription factor forkhead box C1 (FOXC1) promotes metastasis by activating the epithelial to mesenchymal transition; its levels in liver tumors have been associated with shorter survival times of patients. We investigated whether FOXC1 activates inflammation signaling pathways in HCC cell lines. We performed studies in the human HCC cell lines Huh-7 and SMMC7721, as well as the metastatic cell lines MHCC97H and HCCLM3. Cell lines were incubated with IL8 and transcription of reporter genes was measured; cells were also incubated with kinase inhibitors. Levels of FOXC1 or IL8 were knocked down with small interfering mRNAs in Huh7 cells; cells were analyzed in vitro in migration and invasion assays. To study metastasis, HCC cells were injected into flanks of BALB/C nude mice; 4 weeks later the subcutaneous tumor fragments were collected and implanted into livers of the nude mice, and number and size tumors formed were measured. Chromatin immunoprecipitation assays were used to measure binding of transcription factors promoter regions of genes. We measured levels of FOXC1, IL8, CXCR1, and CCL2 in 2 groups of human HCC tissues collected from the Xijing or Tongji Hospitals in China (n=690 and n=312 samples, respectively) using immunohistochemistry. Incubation of HCC cells with IL8 led to increased expression of FOXC1, via activation of PI3K signaling to AKT and HIF1A. Knockdown of FOXC1 in HCC cells that overexpressed IL8 reduced the numbers of metastases formed in mice, compared to cells without FOXC1 knockdown. Transgenic overexpression of FOXC1 in HCC cells with IL8 knockdown increased the numbers of metastases formed in mice, compared with cells without FOXC1 overexpression. CXCR1 and CCL2 were direct transcriptional targets of FOXC1. Knockdown of the combination of CXCR1 and CCL2 reduced the invasive activities of HCC cells that overexpress FOXC1 and formation of lung metastases in mice, whereas transgenic overexpression of CXCR1 increased cell's invasive and metastatic abilities following knockdown of FOXC1. Liver metastases grown from cells that overexpressed FOXC1 were infiltrated by tumor-associated macrophages (TAM), whereas CCL2 knockdown decreased TAM infiltration; depletion of macrophages from mice significantly reduced growth of metastases by cells that overexpressed FOXC1. In human HCC tissues, level of FOXC1 correlated with levels of IL8 and CXCR1 and CCL2 and infiltration of tumors by macrophage. In multivariate analysis, detection of FOXC1 and CCL2 were independent predictors for post-operative recurrence of HCC and overall survival. In HCC cell lines, IL8 activates expression of FOXC1 via the PI3K signaling to AKT and HIF1A. FOXC1 expression leads to trans-activation of CXCR1 and CCL2, promoting inflammation and the invasive and metastatic abilities of HCC cells. Copyright © 2015 AGA Institute. Published by Elsevier Inc. All rights reserved.
    Gastroenterology 06/2015; DOI:10.1053/j.gastro.2015.05.058 · 13.93 Impact Factor
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    ABSTRACT: Multi-drug resistance is the main cause of treatment failure in cancer patients. How to identify molecules underlying drug resistance from multi-omics data remains a great challenge. Here, we introduce a data biased strategy, ProteinRank, to prioritize drug-resistance associated proteins in cancer cells. First, we identified differentially expressed proteins in Adriamycin and Vincristine resistant gastric cancer cells compared to their parental cells using iTRAQ combined with LC-MS/MS experiments, and then mapped them to human protein-protein interaction network; second, we applied ProteinRank to analyze the whole network and rank proteins similar to known drug resistance related proteins. Cross validations demonstrated a better performance of ProteinRank compared to the method without usage of MS data. Further validations confirmed the altered expressions or activities of several top ranked proteins. Functional study showed PIM3 or CAV1 silencing was sufficient to reverse the drug resistance phenotype. These results indicated ProteinRank could prioritize key proteins related to drug resistance in gastric cancer and provided important clues for cancer research.
    Scientific Reports 06/2015; 5:10857. DOI:10.1038/srep10857 · 5.58 Impact Factor
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    ABSTRACT: Esophageal squamous cell carcinoma (ESCC) has a poor prognosis due to its high frequency of metastasis and invasion. Recent studies have suggested glucose-regulated protein 78KD (GRP78) may play important roles in progression and development of malignant tumors. However, the mechanisms of invasion and metastasis of ESCC in relation to GRP78 still remain obscure. The aim of this study was to investigate the effect of GRP78 on invasion and metastasis of ESCC and to explore its potential mechanism. GRP78 expression levels in ESCC tissues were examined by immunohistochemistry. RT-PCR and western blot were used to test the relative expression of GRP78 in non-metastatic and high-metastatic ESCC cells. In vitro and in vivo studies were both performed to investigate the role of GRP78 in invasion and metastasis of ESCC cells. The expression of metastasis-related proteins was examined by western blot in GRP78-depleted cells. The expression of GRP78 is correlated with invasion, metastasis and poor prognosis in ESCC patients. GRP78 expression was significantly higher in highly metastatic cells compared with ESCC non-metastatic cells. In addition, down-regulation of GRP78 significantly inhibited the metastatic potential of ESCC cells in both in vitro and in vivo studies. The expression of MMP-2 and MMP-9 were down-regulated in GRP78-depleted ESCC cells. The present study demonstrated that GRP78 plays important roles in invasion and metastasis of ESCC, indicating that GRP78 might be used as a potential prognostic and therapeutic marker in patients with ESCC by modulating the expression of MMP-2 and MMP-9.
    Digestive Diseases and Sciences 05/2015; DOI:10.1007/s10620-015-3689-6 · 2.55 Impact Factor
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    ABSTRACT: Metastasis, the capability of tumor cells to spread and grow at distant sites, is the main factor in cancer mortality. Because metastasis in sentinel lymph nodes suggests the original spread of tumors from a primary site, the detection of lymph node involvement with cancer serves as an important prognostic and treatment parameter. Here we have developed a panel of DNA aptamers specifically binding to colon cancer cells SW620 derived from metastatic site-lymph node, with high affinity after 14 rounds of selection by the cell-SELEX method. The selected aptamers were subjected to flow cytometry to evaluate their binding affinity. Aptamer XL-33 with the best binding affinity (0.7 nM) and its truncated sequence XL-33-1 with 45 nt showed excellent selectivity for the recognition of target cells SW620. The binding entity of the selected aptamer has been preliminarily determined as a membrane protein on the cell surface. Tissue imaging results showed that XL-33-1 was highly specific to the metastatic tumor tissue or lymph node tissue with corresponding cancer metastasis, and displayed an 81.7% detection rate against colon cancer tissue with metastasis in regional lymph nodes, as well as a 72.4% positive rate against lymph node tissue with colon cancer metastasis. These results suggest that XL-33-1 holds great potential to become a molecular imaging agent for early detection of lymph node tissue with colon cancer metastasis. More importantly, this study clearly demonstrates that metastatic-cell-based SELEX can be used to generate DNA ligands specifically recognizing metastatic cancer cells, which is of great significance for metastatic cancer diagnosis and treatment.
    Analytical Chemistry 04/2015; 87(9). DOI:10.1021/acs.analchem.5b00637 · 5.83 Impact Factor
  • Limin Xia · Kaichun Wu · Daiming Fan
    Gastroenterology 04/2015; 148(4):S-984-S-985. DOI:10.1016/S0016-5085(15)33366-7 · 13.93 Impact Factor
  • Limin Xia · Kaichun Wu · Daiming Fan
    Gastroenterology 04/2015; 148(4):S-1015-S-1016. DOI:10.1016/S0016-5085(15)33471-5 · 13.93 Impact Factor
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    Xingshun Qi · Feifei Wu · Daiming Fan · Guohong Han
    04/2015; 5(2). DOI:10.1016/j.jceh.2015.04.005
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    ABSTRACT: The coagulation abnormalities in non-cirrhotic Budd-Chiari syndrome (NC-BCS) and non-cirrhotic portal vein thrombosis (NC-PVT) are unclear. We conducted this case-control study to investigate the coagulation profile of NC-BCS and NC-PVT in Chinese patients. We measured the levels of factors II, V, VII, VIII, IX, X, XI, XII, protein C (PC), protein S (PS) and antithrombin (AT) in blood samples from 37 NC-BCS patients, 74 NC-PVT patients, and 100 healthy controls. The levels and ratios of pro- and anti-coagulation factors were compared between patients with NC-BCS and healthy controls, between different types of NC-BCS and between NC-PVT and healthy controls. In patients with NC-BCS, factor VIII (P<0.001) was significantly elevated; factor V (P<0.001), VII (P<0.001), IX (P = 0.003), X (P<0.001), XI (P<0.001), XII (P<0.001), PC (P<0.001) and AT (P<0.001) were significantly decreased; and no difference was observed for factor II (P = 0.088) and PS (P = 0.199) compared with healthy controls. Factor VIII-to-PC (P = 0.008), factor VIII-to-PS (P = 0.037) and factor VIII-to-AT (P = 0.001) were significantly increased; other ratios were significantly reduced or did not show any difference. No differences were observed between different types of NC-BCS for individual pro- and anti-coagulation factors or the ratios between them. Among patients with NC-PVT, factor VIII (P<0.001) was significantly elevated and other factors were significantly decreased. Factor II-to-PC (P<0.001), factor VIII-to-PC (P<0.001), factor IX-to-PC (P<0.001), factor VIII-to-PS (P<0.001), factor II-to-AT (P<0.001), factor VIII-to-AT (P<0.001) and factor IX-to-AT (P<0.001) were significantly increased; all other ratios for NC-PVT were significantly reduced or did not show any significant difference. NC-BCS and NC-PVT are associated with elevated levels of factor VIII and the decreased levels of PC and AT were probably the most significant features of coagulation imbalance. Additionally, NC-PVT was associated with decreased levels of PS.
    PLoS ONE 03/2015; 10(3):e0119909. DOI:10.1371/journal.pone.0119909 · 3.23 Impact Factor
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    X Qi · V De Stefano · X Guo · D Fan
    Thrombosis and Haemostasis 03/2015; 113(6). DOI:10.1160/TH14-10-0892 · 5.76 Impact Factor
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    ABSTRACT: This paper aimed to systematically review the survival of Budd-Chiari syndrome and to identify the most robust prognostic predictors. Overall, 79 studies were included. According to the treatment modalities, the median 1-, 5- and 10-year survival rate was 93, 83 and 73% after interventional radiological treatment; 81, 75 and 72.5% after surgery other than liver transplantation; 82.5, 70.2 and 66.5% after liver transplantation and 68.1, 44.4% and unavailable after medical therapy alone. According to the publication years, the median 1-, 5- and 10-year survival rate was 68.6, 44.4% and unavailable before 1990; 75.1, 69.5 and 57% during the year 1991-1995; 77, 69.6 and 65.6% during the year 1996-2000; 86.5, 74 and 63.5% during the year 2001-2005 and 90, 82.5 and 72% after 2006. Bilirubin, creatinine and ascites were more frequently identified as significant prognostic factors in univariate analyses. But their statistical significance was less frequently achieved in multivariate analyses.
    Expert Review of Gastroenterology and Hepatology 03/2015; DOI:10.1586/17474124.2015.1024224 · 2.55 Impact Factor
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    ABSTRACT: Background and study aim: The allocation of sufficient time for trainees to attempt cannulation is necessary for learning and to ensure success with endoscopic retrograde cholangiopancreatography (ERCP) training. However, it is important to balance the benefit to trainee practice against the potential risks to patients. The appropriate time for attempted cannulation by trainees remains unclear. Patients and methods: Three different time limits (5, 10, 15 minutes) were set for cannulation attempts made by four trainees in patients with native papilla undergoing ERCP. Patients were randomly assigned to the 5-, 10-, or 15-minute groups in a 1:1:1 ratio. Rectal indomethacin was used in high-risk patients. The primary outcome was successful cannulation within the allocated time. Secondary outcomes included performance scores, overall success rate, and post-ERCP pancreatitis (PEP). Results: A total of 256 patients were randomly assigned to the 5-minute (n = 84), 10-minute (n = 86), or 15-minute (n = 86) groups. Patients' baseline characteristics were comparable. Success rates for selective bile duct cannulation by trainees were 43.8 %, 75.0 %, and 71.8 % in the 5-, 10-, and 15-minute groups, respectively (P < 0.001). Trainees' self-reported performance scores and video assessment by an independent reviewer were comparable between the 10- and 15-minute groups, which were higher than the 5-minute group (both P < 0.001). Trainers took over the cannulation procedure when trainees did not succeed within the allocated time. There was no significant difference in the overall success rates in cannulation between the three groups. No differences were noted in the use of rectal indomethacin and overall complication rates. Four patients in each group developed PEP (P = 0.996). Conclusion: A time of 10 minutes was considered to be appropriate for trainees to attempt cannulation, with acceptable cannulation success rates and complications.Trial registration: ClinicalTrials.gov number (NCT01851226). © Georg Thieme Verlag KG Stuttgart · New York.
    Endoscopy 03/2015; DOI:10.1055/s-0034-1391564 · 5.20 Impact Factor
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    Yong Lv · Daiming Fan
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    ABSTRACT: Hepatopulmonary syndrome (HPS) is a pulmonary complication observed in patients with chronic liver disease and/or portal hypertension, attributable to an intrapulmonary vascular dilatation that may induce severe hypoxemia. Microvascular dilation and angiogenesis in the lung have been identified as pathologic features that drive gas exchange abnormalities in experimental HPS. Pulse oximetry is a useful screening test for HPS, which can guide subsequent use of arterial blood gases. Contrast-enhanced echocardiography, perfusion lung scanning, and pulmonary arteriography are three currently used diagnostic imaging modalities that identify the presence of intrapulmonary vascular abnormalities. The presence of HPS increases mortality and impairs quality of life, but is reversible with liver transplantation. No medical therapy is established as effective for HPS. At the present time, liver transplantation is the only available treatment for HPS.
    Digestive Diseases and Sciences 03/2015; 60(7). DOI:10.1007/s10620-015-3593-0 · 2.55 Impact Factor
  • X Li · W Liu · H Wang · L Yang · Y Li · H Wen · H Ning · J Wang · L Zhang · J Li · D Fan
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    ABSTRACT: The telomeric protein TRF2, involving in telomeric and extratelomeric DNA damage response, has been previously reported to facilitate multidrug resistance (MDR) in gastric cancer cells by interfering ATM-dependent DNA damage response induced by anticancer drugs. Rap1 is the TRF2-interacting protein in the shelterin complex. Complex formation between Rap1 and TRF2 is essential for their function in telomere and end protection. Here we focus on the effects of Rap1 on TRF2 function in DNA damage response induced by anticancer drugs. Both Rap1 and TRF2 expression were upregulated in SGC7901 and its MDR variant SGC7901/VCR after etoposide treatment, which was more marked in SGC7901/VCR than in SGC7901. Rap1 silencing by siRNA in SGC7901/VCR partially reversed the etoposide resistance. And Rap1 silencing partially reversed the TRF2-mediated resistance to etoposide in SGC7901. Rap1 silencing did not affect the TRF2 upregulation induced by etoposide, but eliminated the inhibition effect of TRF2 on ATM expression and ATM phosphorylation at serine 1981 (ATM pS1981). Furthermore, phosphorylation of ATM targets, including γH2AX and serine 15 (S15) on p53, were increased in Rap1 silencing cells in response to etoposide. Thus, we confirm that Rap1, interacting with TRF2 in the shelterin complex, also has an important role in TRF2-mediated DNA damage response in gastric cancer cells treated by etoposide.
    03/2015; 4(3). DOI:10.1038/oncsis.2015.1
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    ABSTRACT: Portal vein thrombosis (PVT) increases the technical complexity of liver transplantation (LT). This systematic review and meta-analysis aim to analyze the association of pre-LT PVT with the overall survival after LT. PubMed, EMBASE, and Cochrane library databases were used to search for papers related to the association between pre-LT PVT and survival of LT recipients. The differences in the survival rates between the LT recipients with and without pre-LT PVT were expressed as odds ratios (ORs) with 95% confidence intervals (CIs). Twenty-seven papers were included. Overall meta-analysis showed that the total LT recipients with pre-LT PVT had a significantly lower 1-year survival rate than those without pre-LT PVT (OR=0.733, 95%CI=0.621-0.865; P=0.0002). But no statistically significant difference was observed in the in-hospital (OR=0.713, 95%CI=0.343-1.482; P=0.365), 1-month (OR=0.679, 95%CI=0.345-1.333; P=0.261), or 5-year survival rate (OR=0.788, 95%CI=0.587-1.058; P=0.113). Additionally, the 1-year survival rate was significantly lower in the LT recipients with complete PVT than in those without PVT (OR=0.503, 95%CI=0.295-0.858; P=0.012). However, no statistically significant difference in the 1-year survival rate between them was observed in the meta-analysis of high-quality studies (OR=0.899, 95%CI=0.657-1.230; P=0.505) or that of studies in which LT was performed after 2000 (OR=0.783, 95%CI=0.566-1.083; P=0.140). Pre-LT PVT, especially complete PVT, decreased the 1-year survival rate after LT. However, the detrimental effect of pre-LT PVT on the survival of LT recipients became inconclusive in high-quality studies. Additionally, further well-designed cohort studies should validate the association in patients undergoing LT during the latter years.
    Journal of gastrointestinal and liver diseases: JGLD 03/2015; 24(1):51-59. · 1.85 Impact Factor
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    ABSTRACT: Metastasis is the main reason for high recurrence and poor survival of hepatocellular carcinoma (HCC) after curative resection. However, the molecular mechanism underlying HCC metastasis remains unclear. Here we report a novel function of Sox12, a member of SYR-related HMG box (SOX) family proteins, in promoting HCC metastasis. Over-expression of Sox12 was significantly correlated with loss of tumor encapsulation, microvascular invasion, and a higher tumor-nodule-metastasis (TNM) stage, and indicated poor prognosis in human HCC patients. Sox12 expression was an independent and significant risk factor for recurrence and reduced survival after curative resection. Over-expression of Sox12 induced epithelial-mesenchymal transition by trans-activating Twist1 expression. Down-regulation of Twist1 decreased Sox12-enhanced HCC migration, invasion and metastasis, whereas up-regulation of Twist1 rescued the decreased migration, invasion and metastasis induced by Sox12 knockdown. Additionally, serial deletion, site-directed mutagenesis, and chromatin immunoprecipitation assays showed that fibroblast growth factor binding protein 1 (FGFBP1) was a direct transcriptional target of Sox12. Knockdown of FGFBP1 decreased Sox12-mediated HCC invasion and metastasis, whereas over-expression of FGFBP1 rescued the decreased invasion and metastasis induced by Sox12 knockdown. Furthermore, forkhead box Q1 (FoxQ1) directly bound to the Sox12 promoter and trans-activated its expression, which contributed to Sox12 over-expression in human HCC. Knockdown of Sox12 dramatically decreased FoxQ1-mediated HCC metastasis. In two independent cohorts of human HCC tissues, Sox12 expression was positively correlated with Twist1, FGFBP1 and FoxQ1 expression, and patients with positive co-expression of Sox12/Twist1, Sox12/FGFBP1, or FoxQ1/Sox12 were associated with poorer prognosis. Conclusion: Up-regulated Sox12 induced by FoxQ1 promotes HCC invasion and metastasis by trans-activating Twist1 and FGFBP1 expression. Thus, our study implicates Sox12 as a potential prognostic biomarker and a novel therapeutic target for HCC. This article is protected by copyright. All rights reserved. Copyright © 2015 American Association for the Study of Liver Diseases.
    Hepatology 02/2015; 61(6). DOI:10.1002/hep.27756 · 11.19 Impact Factor
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    ABSTRACT: MicroRNAs (miRNAs) are thought to have an important role in tumor metastasis by regulating diverse cellular pathways. Here, we describe the function and regulation network of miR-206 in gastric cancer (GC) metastasis. MiR-206 expression was down-regulated in GC cells especially in high metastatic potential cells, and was also significantly decreased in metastatic lesions compared with their corresponding primary tumor samples. Both gain- and loss-of-function studies confirmed that miR-206 significantly suppressed GC cell invasion and metastasis both in vitro and in vivo. Mechanistically, Paired box3 (PAX3) was identified as a functional target of miR-206 in GC cells. MiR-206 inhibited GC metastasis by negatively regulating expression of PAX3. In addition, PAX3 expression was markedly higher in GC tissues than in adjacent noncancerous tissues. GC patients with positive PAX3 expression had shorter overall survival times. Transwell assays and in vivo metastasis assays demonstrated that overexpression of PAX3 significantly promoted the invasiveness and pulmonary metastasis of GC cells. On the other hand, downregulation of PAX3 markedly reduced cell metastatic potential. Mechanistic investigations indicated that pro-metastasis function of PAX3 was mediated by up-regulating downstream target MET. Moreover, we found that levels of PAX3 and MET were positively correlated in matched human GC specimens, and their coexpression was associated with poor prognoses. In conclusion, our results reveal that miR-206-PAX3-MET signaling is critical to GC metastasis. Targeting the pathway described here may open new therapeutic prospects to restrict the metastatic potential of gastric cancer. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
    Carcinogenesis 02/2015; 36(3). DOI:10.1093/carcin/bgv009 · 5.27 Impact Factor

Publication Stats

7k Citations
2,144.80 Total Impact Points


  • 2000–2015
    • Fourth Military Medical University
      • • State Key Laboratory of Cancer Biology
      • • Department of Gastroenterology
      Xi’an, Liaoning, China
  • 2014
    • Shanghai's Children's Medical Center
      Shanghai, Shanghai Shi, China
  • 2013
    • Shanghai Jiao Tong University
      • Department of Gastroenterology (Children's)
      Shanghai, Shanghai Shi, China
    • The 251st Hospital of Chinese PLA
      Chzhantseyakou, Hebei, China
  • 2012
    • Chinese Academy of Engineering Physics
      Peping, Beijing, China
  • 2011
    • State Key Laboratory of Medical Genetics of China
      Ch’ang-sha-shih, Hunan, China
  • 2008
    • China Academy of Engineering Physics
      Peping, Beijing, China
  • 2007
    • Third Military Medical University
      Ch’ung-ch’ing-shih, Chongqing Shi, China
  • 2004
    • Southern Illinois University Carbondale
      Illinois, United States
  • 2002
    • General Hospital of Jinan Military Region
      Chi-nan-shih, Shandong Sheng, China
  • 2001–2002
    • Southern Medical University
      Shengcheng, Guangdong, China
  • 2000–2001
    • Emory University
      • • Atlanta Veterans Affairs Medical Center
      • • School of Medicine
      Atlanta, Georgia, United States