Daiming Fan

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

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Publications (507)2332.21 Total impact

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    ABSTRACT: This retrospective cohort study aimed to evaluate the prognostic value of the alpha-fetoprotein (AFP) response in advanced-stage hepatocellular carcinoma (HCC) patients treated with sorafenib combined with transarterial chemoembolization. From May 2008 to July 2012, 118 HCC patients with baseline AFP levels >20 ng/ml treated with combination therapy were enrolled. A receiver operating characteristic curve was used to generate a cutoff point for AFP changes for predicting survival. The AFP response was defined as an AFP decrease rate [ΔAFP(%)] greater than the cutoff point. The ΔAFP(%) was defined as the percentage of changes between the baseline and the nadir values within 2 months after therapy. The median follow-up time was 8.8 months (range 1.2–66.9). A level of 46% was chosen as the threshold value for ΔAFP (sensitivity = 53.7%, specificity = 83.3%). The median overall survival was significantly longer in the AFP response group than in the AFP non-response group (12.8 vs. 6.4 months, P = 0.001). Multivariate analysis showed that ECOG ≥ 1 (HR = 1.95; 95% CI 1.24–3.1, P = 0.004) and AFP nonresponse (HR = 1.71; 95% CI 1.15–2.55, P = 0.009) were associated with increased risk of death. In conclusion, AFP response could predict the survival of patients with advanced-stage HCC at an early time point after combination therapy.
    No preview · Article · Feb 2016 · Scientific Reports
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    ABSTRACT: RNAs (miRNAs), through negatively regulating their target genes, influence the development and progression of many cancers. Previously, we found miR-483 was overexpressed in esophageal squamous cell carcinoma (ESCC) tissues, and its overexpression was negatively correlated with the prognosis and positively correlated with multidrug resistance of ESCC, but whether it could affect the biological role of proliferation and migration in ESCC cell lines is unknown. In the present study, we found miR-483-3p was overexpressed in ESCC cell lines as compared with the normal esophageal squamous epithelial cell line. Functional experiments in vitro showed that miR-483-3p could promote the proliferation, migration, transformation of cell cycle from G1 phase to G2 phase of ESCC cells, and could inhibit cells' sensitivity to chemotherapy drugs. Nude mouse tumorigenicity assay indicated that miR-483-3p could promote the growth of ESCC cells in vivo. Western blot assay showed that ectopic expression of miR-483-3p in ESCC cells could downregulate the protein level of etoposide induced 2.4 (EI24), which is a tumor suppressor and hasn't been reported in ESCC. Luciferase reporter assay demonstrated that EI24 was a direct target of miR-483-3p. Collectively, our study demonstrated that miR-483-3p could promote ESCC progression at least in part through directly targeting EI24, supplying a potential strategy for miRNA-based ESCC therapy.
    No preview · Article · Jan 2016 · Cell Biology International
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    ABSTRACT: Clinicopathologic features and clinical outcomes of gastrointestinal stromal tumors (GISTs) in esophagus are limited, because of the relatively rare incidence of esophageal GISTs. Therefore, the aim of the current study was to investigate the clinicopathologic features and clinical outcomes of esophageal GISTs, and to investigate the potential factors that may predict prognosis.Esophageal GIST cases were obtained from our center and from case reports and clinical studies extracted from MEDLINE. Clinicopathologic features and survivals were analyzed and compared with gastric GISTs from our center.The most common location was lower esophagus (86.84%), followed by middle and upper esophagus (11.40% and 1.76%). The majority of esophageal GISTs were classified as high-risk category (70.83%). Mitotic index was correlated with histologic type, mutational status, and tumor size. The 5-year disease-free survival and disease-specific survival were 65.1% and 65.9%, respectively. Tumor size, mitotic index, and National Institutes of Health risk classification were associated with prognosis of esophageal GISTs. Only tumor size, however, was the independent risk factor for the prognosis of esophageal GISTs. In comparison to gastric GISTs, the distribution of tumor size, histologic type, and National Institutes of Health risk classification were significantly different between esophageal GISTs and gastric GISTs. The disease-free survival and disease-specific survival of esophageal GISTs were significantly lower than that of gastric GISTs.The most common location for esophageal GISTs was lower esophagus, and most of the esophageal GISTs are high-risk category. Tumor size was the independent risk factor for the prognosis of esophageal GISTs. Esophageal GISTs differ significantly from gastric GISTs in respect to clinicopathologic features. The prognosis of esophageal GISTs was worse than that of gastric GISTs.
    No preview · Article · Jan 2016 · Medicine
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    ABSTRACT: LAMP2A is the key protein of chaperone-mediated autophagy (CMA), downregulation of LAMP2A leads to CMA blockade. CMA activation has been implicated in cancer growth, but the exact mechanisms are unclear. Elevated expression of LAMP2A was found in 8 kinds of tumors (n=747), suggesting that LAMP2A may have an important role in cancer progression. Unsurprisingly, LAMP2A knockdown in gastric cancer (GC) cells hindered proliferation, accompanied with altered expression of cell cycle-related proteins and accumulation of RND3/RhoE. Interactomic and KEGG analysis revealed that RND3 was a putative CMA substrate. Further study demonstrated that RND3 silencing could partly rescue the proliferation arrest induced by LAMP2A knockdown; RND3 was increased upon lysosome inhibition via both chemicals and LAMP2A-shRNA; Furthermore, RND3 could interact with CMA components HSPA8 and LAMP2A, and be engulfed by isolated lysosomes. Thus, constant degradation of RND3 by CMA is required to sustain rapid proliferation of GC cells. At last, the clinical significance of LAMP2A was explored in 593 gastric noncancerous lesions and 173 GC tissues, the results revealed that LAMP2A is a promising biomarker for GC early warning and prognosis of female GC patients.
    Full-text · Article · Jan 2016 · Autophagy
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    ABSTRACT: Multidrug resistance (MDR) correlates with treatment failure and poor prognosis among gastric cancer (GC) patients. In a previous study using high-throughput functional screening, we identified 11 microRNAs (miRNAs) that regulate MDR in GC and found that miR-508-5p reversed MDR by targeting ABCB1 and ZNRD1. However, the mechanism by which miR-508-5p was decreased in chemo-resistant GC cells was unclear. In this study, we found that ectopic miR-27b is sufficient to sensitize tumors to chemotherapy in vitro and in vivo. Moreover, miR-27b directly targets the 3' untranslated regions (3'-UTRs) of CCNG1, a well-known negative regulator of P53 stability. Interestingly, miR-27b up-regulation leads to increased miR-508-5p expression, and this phenomenon is mediated by CCNG1 and P53. Further investigation indicated that miR-508-5p is directly regulated by P53. Thus, the miR-27b/CCNG1/P53/miR-508-5p axis plays important roles in GC-associated MDR. In addition, miR-27b and miR-508-5p expression was detected in GC tissues with different chemo-sensitivities, and we found that tissues in which miR-27b and miR-508-5p are up-regulated are more sensitive to chemotherapy. Together, these data suggest that the combination of miR-27b and miR-508-5p represents a potential marker of MDR. Restoring the miR-27b and miR-508-5p levels might contribute to MDR reversion in future clinical practice.
    Preview · Article · Dec 2015 · Oncotarget
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    ABSTRACT: Emerging evidence indicates that the neuronal guidance molecule SLIT plays a role in tumor suppression, as SLIT-encoding genes are inactivated in several types of cancer, including lung cancer; however, it is not clear how SLIT functions in lung cancer. Here, our data show that SLIT inhibits cancer cell migration by activating RhoA and that myosin 9b (Myo9b) is a ROBO-interacting protein that suppresses RhoA activity in lung cancer cells. Structural analyses revealed that the RhoGAP domain of Myo9b contains a unique patch that specifically recognizes RhoA. We also determined that the ROBO intracellular domain interacts with the Myo9b RhoGAP domain and inhibits its activity; therefore, SLIT-dependent activation of RhoA is mediated by ROBO inhibition of Myo9b. In a murine model, compared with control lung cancer cells, SLIT-expressing cells had a decreased capacity for tumor formation and lung metastasis. Evaluation of human lung cancer and adjacent nontumor tissues revealed that Myo9b is upregulated in the cancer tissue. Moreover, elevated Myo9b expression was associated with lung cancer progression and poor prognosis. Together, our data identify Myo9b as a key player in lung cancer and as a ROBO-interacting protein in what is, to the best of our knowledge, a newly defined SLIT/ROBO/Myo9b/RhoA signaling pathway that restricts lung cancer progression and metastasis. Additionally, our work suggests that targeting the SLIT/ROBO/Myo9b/RhoA pathway has potential as a diagnostic and therapeutic strategy for lung cancer.
    Full-text · Article · Nov 2015 · The Journal of clinical investigation
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    ABSTRACT: Background and aim: Portal vein thrombosis (PVT) is a frequent event in patients with cirrhosis. The effects of anticoagulation on these patients were still unclear, especially for more advanced PVT. The aim of this study was to retrospectively assess the resolution of PVT and liver disease progression in a large cohort of cirrhotic patients with PVT with or without anticoagulation therapy. Methods: We analyzed data from 66 cirrhotic patients with PVT from January 2002 to June 2014. Thirty patients were anticoagulated with warfarin and 36 patients were untreated. PVT and hepatic decompensation were evaluated. Results: For anticoagulated patients, the thrombosis had improved in 15 (68.2%) patients, was stable in four patients (18.2%), and progressed in three patients (13.6%). For untreated patients, the thrombosis had improved in four patients (25%), was stable in six patients (37.5%), and progressed in six patients (37.5%). The anticoagulation group had significantly better recanalization rates than the untreated group (P=0.011). Degree of superior mesenteric vein (P=0.032, hazard ratio: 15.4; 95% confidence interval: 1.3-200) was a significant predictor. In addition, anticoagulation can effectively improve PVT with a degree less than 75% in the main portal vein compared with untreated patients (6/6 vs. 2/6, P=0.030). The probability of hepatic decompensation at 1 year was 15.6 and 17.9% between the anticoagulation and the untreated groups (P=0.847). Albumin (P=0.06, hazard ratio: 0.860; 95% confidence interval: 0.772-0.959) was a significant predictor. Conclusion: Anticoagulation with warfarin might result in the resolution of more advanced PVT effectively and safely in patients with liver cirrhosis. In addition, we did not demonstrate the benefit of anticoagulation for the decompensation or death.
    Full-text · Article · Oct 2015 · European journal of gastroenterology & hepatology

  • No preview · Article · Oct 2015
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    ABSTRACT: MGd1, a monoclonal antibody raised against gastric cancer cells, possesses a high degree of specificity for gastric cancer (GC). Here we identified that the antigen of MGd1 is CEACAM5, and used MGd1 to investigate the expression of CEACAM5 in non-GC and GC tissues (N=643), as a biomarker for prewarning and prognosis. The expression of CEACAM5 was detected by immunohistochemistry in numerous tissues; its clinicopathological correlation was statistically analyzed. CEACAM5 expression was increased progressively from normal gastric mucosa to chronic atrophic gastritis, intestinal metaplasia, dysplasia and finally to GC (p0.05). In gastric precancerous lesions (intestinal metaplasia and dysplasia), CEACAM5-positive patients had a higher risk of developing GC as compared with CEACAM5-negative patients (OR = 12.68, p0.001). Besides, CEACAM5 was found positively correlated with invasion depth of gastric adenocarcinoma (p0.001). In survival analysis, CEACAM5 was demonstrated to be an independent prognostic predictor for patients with GC of clinical stage IIIA/IV (p=0.033). Our results demonstrate that CEACAM5 is a promising biomarker for GC prewarning and prognostic evaluation.
    No preview · Article · Sep 2015 · Journal of Histochemistry and Cytochemistry
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    ABSTRACT: The strategy of using fecal microbiota transplantation (FMT) for refractory ulcerative colitis (UC) remains unclear if single FMT failed to induce remission. This study aimed to evaluate the efficacy and safety of a designed step-up FMT strategy for the steroid-dependent UC. Fifteen patients with steroid-dependent UC were enrolled, and treated with step-up FMT strategy. Follow-up clinical data was collected for a minimum of 3 months. Fecal microbiota composition before and post FMT of patients and related donors were analyzed by 16S rRNA sequencing. Eight of fourteen (57.1 %) patients achieved clinical improvement and were able to discontinue steroids following step-up FMT. One patient was lost to follow-up. Among the 8 patients who responded, five (35.7 %) received one FMT therapy, one (7.1 %) received two FMTs, and two (14.2 %) received two FMTs plus a scheduled course of steroids. Four (28.6 %) of the 8 patients who responded maintained long-term remission during follow-up (3–18 months). Six patients (42.9 %) failed to meet the criteria of clinical improvement and maintained steroid dependence, though three experienced transient or partial improvement. Microbiota analysis showed that FMT altered the composition greatly, and a microbiota composition highly similar to that of the donor emerged in the patients with successful treatment. No severe adverse events occurred during treatment and follow-up. Step-up FMT strategy shows promise as a therapeutic strategy for patients with steroid-dependent UC, likely due to the successful restructuring of gut microbial composition. Trial registration: ClinicalTrials.gov, Number NCT01790061
    Preview · Article · Sep 2015 · Journal of Translational Medicine
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    Yong Lv · Daiming Fan

    Full-text · Dataset · Aug 2015
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    ABSTRACT: The effect of chemotherapy of gastric cancer (GC) remains very poor because of multidrug resistance (MDR). However, the mechanisms underlying MDR of GC remains far from fully understood. The aim of this study is to illustrate the potential mechanisms of the MDR of GC at mainly the long non-coding RNA (lncRNA) level. In this study, GC cell line, SGC7901, and two MDR sublines, SGC7901/VCR and SGC7901/ADR were subjected to an lncRNA microarray analysis. Bioinformatics and verification experiments were performed to investigate the potential lncRNAs involved in the development of MDR. Pathway analysis indicated that 15 pathways corresponded to down-regulated transcripts and that 20 pathways corresponded to up-regulated transcripts (p-value cut-off is 0.05). GO analysis showed that the highest enriched GOs targeted by up-regulated transcripts were "system development" and the highest esenriched GOs targeted by the down-regulated transcripts were "sterol biosynthetic process". Our study is the first to interrogate differentially expressed lncRNAs in human GC cell line and MDR sublines and indicates that lncRNAs are worthwhile for further study to be the novel candidate biomarkers for the clinical diagnosis of MDR and potential targets for further therapy.
    Preview · Article · Aug 2015 · PLoS ONE
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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.
    Full-text · Article · Aug 2015 · Liver international: official journal of the International Association for the Study of the Liver
  • 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.
    No preview · Article · Jul 2015 · Expert Opinion on Therapeutic Targets
  • 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.
    No preview · Article · Jun 2015 · Expert review of gastroenterology & hepatology
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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.
    No preview · Article · Jun 2015 · Gastroenterology
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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.
    Preview · Article · Jun 2015 · Scientific Reports
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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.
    No preview · Article · May 2015 · Digestive Diseases and Sciences
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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.
    Full-text · Article · Apr 2015 · Analytical Chemistry
  • Limin Xia · Kaichun Wu · Daiming Fan

    No preview · Article · Apr 2015 · Gastroenterology

Publication Stats

9k Citations
2,332.21 Total Impact Points


  • 2001-2016
    • Fourth Military Medical University
      • • State Key Laboratory of Cancer Biology
      • • Department of Gastroenterology
      Xi’an, Liaoning, China
  • 2013-2014
    • Shanghai Jiao Tong University
      • Department of Gastroenterology (Children's)
      Shanghai, Shanghai Shi, 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
  • 2002-2006
    • Southern Medical University
      Shengcheng, Guangdong, China
  • 2000-2001
    • Emory University
      • School of Medicine
      Atlanta, Georgia, United States