Xiu-E Xu

Shantou University, Swatow, Guangdong, China

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Publications (23)60.36 Total impact

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    ABSTRACT: Focal distribution of microvascular and lymphatic vessels is a critical issue in cancer, and is measured by tissue microarray (TMA) construction from paraffin-embedded surgically obtained tissues, a process that may not accurately reflect true focal distribution. The aim of this study was to assess the concordance of microvascular density (MVD) and lymphatic vessel density (LVD) in TMAs with corresponding whole sections, and to correlate the MVD or LVD with clinicopathological parameters in 124 cases of esophageal squamous cell carcinoma (ESCC). MVD, determined by CD105 immunohistochemistry of whole sections, was strongly associated with lymph node metastasis (p=0.000) and pTNM stage (p=0.001). Kaplan-Meier survival analysis showed that increasing CD105 microvessel count correlated with decreasing survival (p<0.001). The same result was acquired when MVD was calculated from tissue microarrays. Analysis of continuous data showed a highly significant correlation between whole sections and TMA data (Pearson r=0.522, p<0.001). Increasing LVD, as determined by D2-40 immunohistochemistry of whole sections, correlated with decreasing survival, but this relationship was undetectable using TMAs. In conclusion, we demonstrate that for the selected endothelial markers, TMAs can provide a realistic and reliable estimate of the extent of MVD, but not LVD in ESCC samples.
    Acta histochemica 01/2014; · 1.61 Impact Factor
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    ABSTRACT: As a member of catenin family, expression of δ-catenin and its clinical implication in numerous tumors remains unclear. In the present study, expression of δ-catenin in esophageal squamous cell carcinoma (ESCC) and its correlations with patient prognosis were explored. We detected the expression of δ-catenin, by immunohistochemistry, in ESCC tissues from 299 cases, and analyzed the correlation between δ-catenin expression and patient clinicopathological features. Compared with a lack of expression in adjacent normal esophageal epithelium (0%, 0/47), the frequency of δ-catenin protein was increased in ESCC tissues to 41.5% (124/299, P < 0.001), and expression correlated with TNM stage and lymph node metastasis (P =0.025 and 0.019, respectively). Furthermore, Kaplan-Meier survival analysis revealed that patients with high δ-catenin expression had shorter survival than patients with low expression (P = 0.010), and multivariate Cox analysis revealed that high δ-catenin expression was also an independent prognostic factor (P = 0.001). In Transwell assays, migration of ESCC cells was enhanced by δ-catenin overexpression, whereas proliferation of ESCC cells was unchanged. Together, our results suggest that δ-catenin acts as an oncoprotein when overexpressed in ESCC, and its expression is associated with poor prognosis and malignant cell behavior.
    Human pathology 01/2014; · 3.03 Impact Factor
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    ABSTRACT: The adapter protein growth factor receptor-bound 2 (GRB2) is essential for various basic cellular functions by mediating the regulation of receptor tyrosine kinase (RTK) signaling, however, little is known about GRB2 expression in esophageal squamous cell carcinoma (ESCC). We sought to characterize GRB2 expression and its relationship with clinicopathological parameters and prognostic significance in ESCC patients. Here, it was presented that GRB2 was overexpressed in cytoplasm in 58.1% (100/172) of ESCC cases by immunohistochemistry. Survival analysis demonstrated overexpression of GRB2 protein was significantly related to poor prognosis of ESCC patients (P = 0.021). Furthermore, overexpression of GRB2 was significantly associated with the lymph node metastases. In addition, subgroup analysis according to lymph node metastasis revealed a shorter disease-free survival (DFS) in the ESCC patients with GRB2 overexpression than the patients with GRB2 low-expression (Means for DFS months: 33.8 versus 52.1). Finally, the significant difference between overexpression of GRB2 and poor survival rates exhibited in univariate analysis (P = 0.022) and multivariate Cox analysis (close to significance, P = 0.065), demonstrated that GRB2 was an independent factor in prognosis of ESCC patients. In conclusion, GRB2 expression status could be as a positive biomarker of ESCC progression and lymph node metastasis.
    International journal of clinical and experimental pathology. 01/2014; 7(6):3132-40.
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    ABSTRACT: Desmoglein 3 (DSG3), a transmembrane cadherin of the desmosomal cell–cell adhesion structure, plays vital roles in the maintenance of normal epithelial tissue architecture. Reports implicating a role for DSG3 expression in cancer are few and contradictory. In this study, immunohistochemical staining was employed to investigate DSG3 expression and subcellular localization in esophageal squamous cell carcinoma (ESCC), and to correlate changes with clinical characteristics. Results indicate that in normal squamous cell epithelia, strong DSG3 immunoreactivity was observed in the Stratum spinosum, and localization occurred only at the cell membrane. In ESCC, DSG3 immunoreactivity displayed an abnormal cytoplasmic localization that was correlated with cell differentiation (P = 0.018). Most strikingly, in 74.1% of the tumors, DSG3 expression was up-regulated and correlated with regional lymph node metastasis (P = 0.036). Moreover, in patients without lymph node metastasis, cytoplasmic localization of DSG3 correlated with poor prognosis (P = 0.044). These results suggest that DSG3 is involved in the development of ESCC and imply that DSG3 overexpression is likely to be an essential contributor to the aggressive features of esophageal cancer.
    Acta histochemica 01/2014; · 1.61 Impact Factor
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    ABSTRACT: Esophageal squamous cell carcinoma (ESCC) has the highest mortality rates in China. The 5-year survival rate of ESCC remains dismal despite improvements in treatments such as surgical resection and adjuvant chemoradiation, and current clinical staging approaches are limited in their ability to effectively stratify patients for treatment options. The aim of the present study, therefore, was to develop an immunohistochemistry-based prognostic model to improve clinical risk assessment for patients with ESCC.
    PLoS ONE 01/2014; 9(8):e106007. · 3.53 Impact Factor
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    ABSTRACT: To further our understanding of the pathobiology of esophageal squamous cell carcinoma (ESCC), we previously performed miRNA profiling that revealed downregulation of miR-200b in ESCC. Using quantitative qRT-PCR applied to 88 patient samples, we confirmed that ESCC tumors expressed significantly lower levels of miR-200b compared to the respective adjacent benign tissues (P = 0.003). Importantly, downregulation of miR-200b significantly correlated with shortened survival (P = 0.025), lymph node metastasis (P = 0.002) and advanced clinical stage (P = 0.020) in ESCC patients. Quantitative mass spectrometry identified 57 putative miR-200b targets, including Kindlin-2, previously implicated in the regulation of tumor invasiveness and actin cytoskeleton in other cell types. Enforced expression of miR-200b mimic in ESCC cells led to a decrease of Kindlin-2 expression, whereas transfection of miR-200b inhibitor induced Kindlin-2 expression. Furthermore, transfection of miR-200b mimic or knockdown of Kindlin-2 in ESCC cells decreased cell protrusion and focal adhesion formation, reduced cell spreading and invasiveness/migration. Enforced expression of Kindlin-2 largely abrogated the inhibitory effects of miR-200b on ESCC cell invasiveness. Mechanistic studies revealed that Rho-family GTPases and focal adhesion kinase mediated the biological effects of the miR-200b - Kindlin-2 axis in ESCC cells. To conclude, loss of miR-200b, a frequent biochemical defect in ESCC, correlates with aggressive clinical features. The tumor suppressor effects of miR-200b may be due to its suppression of Kindlin-2, a novel target of miR-200b that modulates actin cytoskeleton, focal adhesion formation and the migratory/invasiveness properties of ESCC.
    Carcinogenesis 09/2013; · 5.64 Impact Factor
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    ABSTRACT: In contrast to the well recognized loss of adherens junctions in cancer progression, the role of desmosomal components in cancer development has not been well explored. We previously demonstrated that desmocollin-2 (DSC2), a desmosomal cadherin protein, is reduced in esophageal squamous cell carcinoma (ESCC), and is associated with enhanced tumour metastasis and poor prognosis. Here, we report that restoration of DSC2 in ESCC cells impeded cell migration and invasion both in vitro and in vivo, whereas siRNA-mediated suppression of DSC2 expression increased cell motility. In E-cadherin-expressing ESCC cells, DSC2 restoration strengthened E-cadherin-mediated adherens junctions and promoted the localization of β-catenin at these junctions, which indirectly inhibited β-catenin-dependent transcription. These effects of DSC2 were not present in EC109 cells that lacked E-cadherin expression. ESCC patients, with tumours that had reduced E-cadherin and negative DSC2, had poorer clinical outcomes than patients with tumours that lacked either E-cadherin or DSC2, implying that invasive potential of ESCC cells was restricted by both DSC2 and E-cadherin-dependent junctions. Further studies revealed that DSC2 was a downstream target of miR-25. Enhanced miR-25 promoted ESCC cell invasiveness, whereas restoration of DSC2 abolished these effects. Collectively, our work suggests that miR-25-mediated down-regulation of DSC2 promotes ESCC cell aggressiveness through redistributing adherens junctions and activating beta-catenin signaling.
    The Journal of Pathology 07/2013; · 7.59 Impact Factor
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    ABSTRACT: Opioid receptors, members of the G-protein-coupled receptor superfamily, appear to be involved in cancer progression. However, the expression and significance of opioid receptors in esophageal squamous cell carcinoma (ESCC) remain unclear. In this study, we demonstrated by flow cytometry that μ, δ, and κ-opioid receptors (MOR, DOR, and KOR) are expressed to various degrees in ESCC cell lines. The KOR protein was further examined by several methods in ESCC cell lines and tissues. Immunocytochemical staining localized KOR to the cell membrane in KYSE180 cells and the nucleus in EC109 cells, whereas no signal or weak staining of the cytoplasm was observed in KYSE150 cells. The expression of KOR was confirmed in ESCC cells by Western blotting. Furthermore, immunohistochemistry staining showed that KOR was up-regulated in ESCC tissues compared with nontumorous esophageal epithelium (P = .004, χ(2) test). Moreover, high nuclear KOR expression was significantly correlated with lymph node metastasis in 256 ESCC cases (R = 0.144; P = .030, Kendall τB test). Patients with high nuclear KOR expression in ESCC had a significantly poorer prognosis (P = .001, log-rank test). Multivariate Cox analysis revealed that KOR in the nucleus was an independent prognostic factor (hazard ratio, 1.789; 95% confidence interval, 1.177-2.720; P = .006). Our results suggest that KOR is involved in the carcinogenesis or progression of ESCC and that nuclear KOR may be indicative of prognosis.
    Human pathology 04/2013; · 3.03 Impact Factor
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    ABSTRACT: Endogenous soluble vascular endothelial growth factor receptor-2 (esVEGFR-2), a new splicing variant of VEGFR-2, was shown to be the first endogenous specific inhibitor of lymphatic vessel growth. The expression of esVEGFR-2 and its clinicopathological roles in esophageal squamous cell carcinoma (ESCC) are unclear. In this article, quantitative RT-PCR was employed to detect the mRNA levels of esVEGFR-2 and VEGF-C in 90 paired primary ESCC tissues, along with immunohistochemical staining to measure esVEGFR-2 protein in 182 ESCC primary tissues. Correlations between esVEGFR-2 expression and clinicopathological features were also analyzed. Compared with the corresponding non-neoplastic esophageal mucosa tissues, the mRNA level of esVEGFR-2 was decreased, whereas the mRNA level of VEGF-C was increased in ESCCs. Downregulation of esVEGFR-2 mRNA level was significantly correlated with pTNM stages (χ2 = 7.790, p=0.02). Immunohistochemical staining of esVEGFR-2 was inclined to be reduced in ESCC tissues; lower esVEGFR-2 protein expression was related to better prognosis (χ2 = 6.366, p=0.012), whereas higher esVEGFR-2 protein accumulation in ESCC tissues was an independent prognostic factor for poor survival of patients (hazard ratio, 1.606; 95% confidence interval, 1.042–2.476; p=0.032). Taken together, altered expression of esVEGFR-2 is correlated with progression of ESCC. esVEGFR-2 might serve as a new independent prognostic marker for ESCC patients.
    Journal of Histochemistry and Cytochemistry 02/2013; · 2.26 Impact Factor
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    ABSTRACT: Gene amplified in squamous cell carcinoma 1 (GASC1) is a member of Jumonji C-domain containing histone demethylases that play an essential role in affecting chromatin architecture and gene expression. The purpose of this study was to determine the expression features and the clinical significance of GASC1 in esophageal squamous cell carcinoma (ESCC). GASC1 expression was detected on tissue microarrays of ESCC samples in 185 cases using immunohistochemical staining. Strong nuclear staining for GASC1 was observed in a subset of ESCC samples. The nuclear expression of GASC1 was significantly associated with lymph node metastasis (P=0.030) and tumor-node metastasis stages (P=0.013). Kaplan-Meier survival analysis showed a tendency that high expression of GASC1 in the nucleus was associated with poor survival of ESCC patients, with a 5-year survival rate of 26.5%, as compared to 43.7% for patients with GASC1-negative/low expression. Furthermore, multivariate analysis revealed that high expression of GASC1 likely acts as a predictive factor for overall survival of ESCC patients, despite the P-value failing to reach significance (P=0.059). The findings indicate that histone demethylase GASC1 may play an important role in promoting cancer metastasis, and shed new light on the importance of targeting GASC1 to suppress metastatic disease in various tumor types, including ESCC.
    American Journal of Cancer Research 01/2013; 3(5):509-17. · 2.65 Impact Factor
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    ABSTRACT: This study investigated the distribution of neutrophil gelatinase-associated lipocalin (NGAL) and neutrophil gelatinase-associated lipocalin receptor (NGALR) in human embryonic, fetal and normal adult tissues. Tissue microarray technology was used to perform immunohistochemical examination on human embryos, fetuses at 4-22 weeks of gestation and adult tissue specimens. Results demonstrated that during the development of the nervous system, NGALR was prevalent in the neural tube and cerebrum, and NGAL was only detected in the stellate cells of the cerebrum and the Purkinje cells of the cerebellum. NGAL and NGALR were expressed in the lung alveolar epithelium and in the gastrointestinal tract in embryos, but were almost undetectable in later developmental stages. In the embryonic adrenal glands, the two proteins demonstrated moderate positivity in the cortex and the medulla. In adults, NGAL was particularly present in the cells of the inner and outer layers of the cortex and was absent in the medulla, while NGALR exhibited strong positivity in the cortex and the medulla. Evident expression of NGAL and NGALR was observed throughout development in the neutrophil-rich sites, the renal tubule epithelium and certain gland epithelia of the gastrointestinal tract, but was undetectable in the heart, liver and thyroid gland. Taken together, these results demonstrated that the expression of NGAL and NGALR was time-specific and highly tissue‑specific. Correlations between their expression in embryogenesis and carcinogenesis should be examined.
    Molecular Medicine Reports 07/2012; 6(4):716-22. · 1.17 Impact Factor
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    ABSTRACT: Jumonji AT-rich interactive domain 1B (JARID1B) and PHD finger protein 2 (PHF2), members of the histone demethylases, have been found to be involved in many types of tumors. However, the expression and prognostic significance of JARID1B and PHF2 in esophageal squamous cell carcinoma (ESCC) still remains unclear. In this study, JARID1B and PHF2 expression were detected on tissue microarrays of ESCC samples in 120 cases using immunohistochemical staining. Our results showed that JARID1B and PHF2 were overexpressed in ESCCs. In addition, a significant correlation was observed between JARID1B nuclear expression level and histological grade (P=0.003). Kaplan-Meier survival analysis showed a tendency that high cytoplasmic expression of JARID1B and PHF2 was associated with decreased overall survival of ESCC patients, whereas JARID1B high expression in the nucleus was associated with high overall survival, although there was no statistical significance. Overall, our data suggest that JARID1B and PHF2 are overexpressed in ESCC and that they may play crucial roles in the course of ESCC initiation and/or progression.
    Acta histochemica 04/2012; · 1.61 Impact Factor
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    ABSTRACT: Sigma1 receptor (sigma1R), a significant protein, has been found to be frequently upregulated in human tumor cells and tissues. It has been demonstrated that sigma1R is involved in proliferation and adhesion of cancer cells. However, the significance of sigma1R expression in esophageal squamous cell carcinoma (ESCC) remains unclear. In this article, by a series of methods, the authors examined the expression of sigma1R protein in ESCC cell lines and tissues. Flow cytometry indicated intense staining of sigma1R in ESCC cells. Immunocytochemistry staining demonstrated that sigma1R was mainly distributed in cytoplasm and nucleus in ESCC cell lines. Western blotting was performed to characterize the relative expression of sigma1R in different ESCC cell lines. Moreover, different levels of sigma1R were presented from normal epithelium to carcinoma by immunohistochemistry analysis, which demonstrated that sigma1R was highly expressed in tumors. Association analysis showed significant correlations between total sigma1R protein levels and pathologic TNM (pTNM) classification of tumors (r=0.216, p=0.011). Furthermore, the sigma1R in the nucleus was significantly correlated with pTNM classification and lymph node metastasis (r=0.263, p=0.002, and r=0.269, p=0.002, respectively). These data indicated that sigma1R may serve as a potential predictive factor for pTNM classification and tumor development in ESCC.
    Journal of Histochemistry and Cytochemistry 04/2012; 60(6):457-66. · 2.26 Impact Factor
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    ABSTRACT: Lysyl oxidase family members have various roles in cancer progression. The aim of this study was to investigate their expression and clinical significance in esophageal squamous cell carcinoma. We examined messenger RNA expression of lysyl oxidase family members including lysyl oxidase and lysyl oxidase-like proteins (lysyl oxidase L) in 10 esophageal squamous cell carcinoma cell lines and 83 pairs of tumor samples by quantitative real-time polymerase chain reaction. All except lysyl oxidase L3 were expressed at high levels in esophageal squamous cell carcinoma, but only lysyl oxidase L2 was associated with lymph node metastasis (P = .034). We examined lysyl oxidase L2 protein further by immunohistochemistry staining in 178 surgically resected esophageal squamous cell carcinoma tissue samples. The protein manifested decreased nuclear expression and increased cytoplasmic expression. Moreover, these 2 events both had significant correlation with the presence of lymph node metastasis (P = .001 and P < .001). Overall survival rates of the patients with esophageal squamous cell carcinoma with decreased nuclear expression or increased cytoplasmic expression of lysyl oxidase L2 were significantly lower than those of the patients with esophageal squamous cell carcinoma with the reverse expression pattern (P = .040 or P = .022). Multivariate analyses revealed that nuclear expression of lysyl oxidase L2 was an independent prognostic factor for esophageal squamous cell carcinoma. These results suggest that lysyl oxidase L2 exerts a critical effect on esophageal squamous cell carcinoma progression and can be a predictive marker of lymph node metastasis and outcome.
    Human pathology 12/2011; 43(7):1068-76. · 3.03 Impact Factor
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    ABSTRACT: Ezrin, which cross-links the cytoskeleton and plasma membrane, was involved in a wide variety of cellular processes. Here, to investigate the distribution of ezrin, tissue microarray technology was employed to perform immunohistochemical experiments on human embryos, fetuses at 4 to 22 weeks' gestation, and adult tissue specimens. Results showed that ezrin was widely expressed in the gastrointestinal tract throughout the human developmental stages studied. At 6 to 8 weeks' gestation, ezrin was found in epithelial cells, and this staining pattern was particularly pronounced in the brush border of mature absorptive cells lining the villus in later developmental stages and adult tissues. Throughout neural development, ezrin was only expressed in the neural tube at 4 weeks' gestation. Ezrin was also detected in the cortex and medulla of the adrenal gland at 8 to 12 weeks' gestation, whereas its immunoreactivity was increased from the zona glomerulosa through the zona reticularis and was essentially undetectable in the adrenal medulla of adult tissues. Significant expression of ezrin was seen throughout development in the kidney, spleen, lymph nodes, and cells of stratified squamous epithelia. However, ezrin was undetectable in lung, liver, heart, and blood vessels. These results demonstrated that the expression pattern of ezrin was highly time specific and tissue specific.
    Journal of Histochemistry and Cytochemistry 08/2011; 59(11):1001-8. · 2.26 Impact Factor
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    ABSTRACT: The aim of this study was to evaluate HDPR1 expression in esophageal squamous cell carcinoma (ESCC) and the relationship between HDPR1 and beta-catenin by immunohistochemical analysis. The clinical relevance of these proteins was also analyzed. Immunohistochemistry was performed on paraffin-embedded tissue specimens from 184 ESCC patients to detect the expression of HDPR1 and beta-catenin. The correlation between the results of immunoexpression and the clinicopathologic features was processed statistically. Increased cytoplasmic and nuclear HDPR1 expression was noted in 100 (54.3%) and 131 (71.2%) of 184 specimens, respectively. Statistical analysis showed significant associations of cytoplasmic HDPR1 with regional lymph node metastasis (p = 0.021) and P-stage (p = 0.004). The increased nuclear staining was only correlated with P-stage (p = 0.047). Significant associations of coexpression of cytoplasmic and nuclear HDPR1 with regional lymph node metastasis (p = 0.015) or P-stage (p = 0.002) were observed. Enhanced cytoplasmic expression of HDPR1 was positively correlated with increased cytoplasmic but not reduced membranous beta-catenin expression (r = 0.239, p = 0.027 and r = 0.126, p = 0.089, respectively). These finding suggested that cytoplasmic HDPR1 protein expression was associated with tumor malignant progression via beta-catenin accumulation. It implicated that cytoplasmic HDPR1 expression may serve as a potential predictive factor for lymph node metastasis and tumor development in ESCC.
    Journal of Histochemistry and Cytochemistry 04/2011; 59(7):711-8. · 2.26 Impact Factor
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    ABSTRACT: Ezrin, a member of the ezrin-radixin-moesin family, was implicated in tumor progression, metastatic dissemination, and adverse outcomes in several cancer types, including esophageal squamous cell carcinoma (ESCC). The purpose of this study was to explore the clinical significance of ezrin expression in ESCC. Ezrin expression was detected on tissue microarrays of ESCC samples in 307 cases using immunohistochemical staining. Survival analysis was assessed by the Kaplan-Meier analysis. Relative risk was evaluated by the multivariate Cox proportional hazards model. The staining pattern of ezrin was heterogeneous and varied from negative/weakly to intense expression in a cytoplasmic distribution. Kaplan-Meier survival analysis showed that ezrin expression was related to poor overall survival of ESCC patients (P=0.023). Further analysis revealed that ezrin expression was associated with the survival in the cases of stage III/IV (P=0.002); but did not influence the survival in the patients of stage I/II. Multivariate Cox analysis demonstrated that ezrin was an independent factor in prognosis of ESCC (P=0.011). Ezrin might be a new molecular marker to predict the prognosis of ESCC patients.
    Journal of Surgical Oncology 03/2011; 104(5):538-43. · 2.64 Impact Factor
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    ABSTRACT: Previous studies have shown that neutrophil gelatinase-associated lipocalin (NGAL) is overexpressed in oesophageal squamous cell carcinoma (ESCC) and closely associated with the invasiveness of ESCC cells. Recently, NGAL receptor (NGALR) was identified from ESCC cells, and was also found to be increased in ESCC. The purpose of this study was to reveal the clinical significance of NGAL and/or NGALR in ESCC. Tissue microarray was performed to detect expression of NGAL and NGALR in 222 ESCC specimens. Pearson χ(2) test was used to analyse correlations between NGAL and/or NGALR expression and clinicopathological features. Kaplan-Meier survival curves and the Cox proportional hazards regression model were used to evaluate the effect of NGAL and/or NGALR expression on prognosis of patients with ESCC. NGAL and NGALR were highly expressed in ESCC. χ(2) test results showed no significant correlations between NGAL or NGALR expression and clinicopathological features. However, NGAL/NGALR coexpression correlated with histological differentiation grade (p=0.033). Survival analysis showed that positive expression of NGAL or NGALR was significantly associated with a poor prognosis for patients with ESCC (p=0.000 or p=0.002). Patients with positive expression of both NGAL and NGALR had a shorter survival time than those with negative expression of both (p=0.048). Multivariate analysis showed that both NGAL and NGALR were independent prognostic factors. These results indicate that both NGAL and NGALR may be involved in the progression of ESCC and can be considered as independent prognostic factors of ESCC.
    Journal of clinical pathology 01/2011; 64(1):69-74. · 2.43 Impact Factor
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    ABSTRACT: Phosphorylation of fascin at serine 39 (phospho-S39-fascin) could inhibit its actin-binding and actin-bundling activities and decrease filopodia formation. However, the relationship between phospho-S39-fascin expression and clinicopathological parameters in tumors is still unknown. Here, Western blot analysis and IHC applied to tissue microarray technology were performed to examine the expression status of non-phosphorylated fascin (fascin) and phospho-S39-fascin and their impacts on the prognosis of patients with esophageal squamous cell carcinoma (ESCC). Fascin and phospho-S39-fascin expressions were tested by cytoplasmic staining. Among the 254 patients, 90 cases showed high expression of fascin and 87 cases showed high expression of phospho-S39-fascin. Survival analysis showed that high expression of fascin was significantly associated with a poor prognosis of the patients with ESCC (p=0.004). In contrast, high expression of phospho-S39-fascin correlated significantly with an improved outcome of patients (p=0.020). Multivariate analysis showed that both fascin and phospho-S39-fascin were independent prognostic factors. In a combined analysis, the patients with high expression of fascin and low expression of phospho-S39-fascin tumors had a shorter overall survival than those with high expression of both fascin and phospho-S39-fascin tumors (5-year overall survival rate: 28.7% vs 48.3%, p=0.068). Our results suggest that high expression of fascin correlates with poor outcome and that high expression of phospho-S39-fascin decreases the risk of poor prognosis in ESCC. This manuscript contains online supplemental material at http://www.jhc.org. Please visit this article online to view these materials.
    Journal of Histochemistry and Cytochemistry 11/2010; 58(11):979-88. · 2.26 Impact Factor
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    ABSTRACT: Desmocollin 2, a desmosomal component, is a key membrane glycoprotein critically involved in cell-cell adhesion and the maintenance of normal tissue architectures in epithelia. Reports exploring the link of desmocollin expression to cancers are limited. The aim of this study was to investigate the expression of desmocollin 2 in esophageal squamous cell carcinoma and, in particular, to determine the extent to which the patterns of desmocollin 2 expression correlated with the clinical parameters. Desmocollin 2 expression was evaluated in 308 cases of esophageal squamous cell carcinoma using immunohistochemistry. Western blotting and reverse transcriptase polymerase chain reaction were performed to characterize the relative expression levels of desmocollin 2 isoforms. The results indicated that desmocollin 2 expression was reduced significantly in esophageal cancer in both protein and messenger RNA levels and that this reduction was associated with poor survival (P = .011). The expression of desmocollin 2 was prominent in normal esophageal epithelia and highly differentiated esophageal tumors, but was reduced or absent in poorly differentiated tumor specimens. Furthermore, in 74.7% of tumor tissues, desmocollin 2 immunoreactivity displayed an abnormal cytoplasmic localization that was correlated with poor tumor differentiation (P < .001), regional lymph node metastasis (P < .001), pathologic tumor-node-metastasis stages (P < .001), and poor prognosis (P = .048). Multivariate analysis showed that desmocollin 2 expression level was an independent prognostic factor for esophageal squamous cell carcinoma. These data suggest that desmocollin 2 is involved in the transformation and development of esophageal tumors and that desmocollin 2 expression level and intracellular localization may serve as a predictor for patient outcomes.
    Human pathology 10/2010; 41(10):1456-65. · 3.03 Impact Factor