Qianze Dong

China Medical University (PRC), Shenyang, Liaoning, China

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Publications (11)32.85 Total impact

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    ABSTRACT: Previous study indicated diversin overexpression in human cancers. However, its expression pattern in human gliomas and the molecular mechanisms of diversin on cancer progression have not been characterized. In the present study, diversin expression was investigated in 105 glioma specimens using immunohistochemistry. Negative staining was observed in normal glial cells, and positive staining was found in 33 out of 105 (31.4 %) glioma specimens. Diversin overexpression correlated with advanced tumor grade (p < 0.05). Small interfering RNA (siRNA) knockdown was performed in U87 and TG905 cell lines with high endogenous diversin expression. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and colony formation assay showed that diversin knockdown inhibited glioma cell growth. Matrigel invasion assay showed that diversin depletion inhibited cell invasion. In addition, messenger RNA (mRNA) and protein levels of matrix metallopeptidase 9 (MMP9) were downregulated after siRNA treatment. In conclusion, diversin is overexpressed in human glioma and regulates glioma cell proliferation and invasion, possibly through MMP9.
    Tumor Biology 05/2014; · 2.52 Impact Factor
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    ABSTRACT: Diversin was recently reported to play roles in Wnt and JNK pathways. However, the expression pattern and biological roles of diversin in human breast cancer have not been reported. In the present study, we found that diversin was overexpressed in breast cancer specimens by immunohistochemistry and western blot. Significant association was observed between diversin overexpression and TNM stage (p = 0.0036), nodal metastasis (p = 0.0033), negative estrogen receptor expression (p = 0.0012) and triple-negative status (p = 0.0017). Furthermore, colony formation assay and matrigel invasion assay showed that knockdown of diversin expression in MDA-MB-231 cell line with high endogenous expression decreased cell proliferation and cell invasion. Transfection of diversin plasmid in MCF-7 cell line increased cell proliferation and invasion. Further analysis showed that diversin depletion downregulated JNK phosphorylation while its overexpression upregulated JNK phosphorylation. In conclusion, our study demonstrated that diversin was overexpressed in human breast cancers. Diversin could contribute to breast cancer cell proliferation and invasion.
    PLoS ONE 01/2014; 9(5):e98591. · 3.73 Impact Factor
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    ABSTRACT: To investigate the expression pattern of SPAG9 protein and its clinical significance in human non-small cell lung cancer (NSCLC). We checked a panel of 120 NSCLC tissues and 20 corresponding normal lung tissues by immumohistochemistry. We observed negative staining in the normal bronchial epithelia and positive staining of SPAG9 in 63 out of 120 (52.5%) NSCLC samples. Overexpression of SPAG9 correlated with poor tumor differentiation (p=0.002), advanced p-TNM stage (p=0.0001), nodal metastasis (p=0.0061) and poor overall survival (p=0.0001). We silenced SPAG9 gene in A549 and H1299 cells by specific siRNA and found that silencing SPAG9 expression inhibited cell growth and invasion. In addition, the protein and mRNA levels of MMP9 were also down-regulated in SPAG9 knocked down cells. Further research demonstrated SPAG9 depletion could inhibit the activity of p-JNK. In conclusion, SPAG9 might act as an important promoter in lung cancer progression and invasion via MMP9 regulation and JNK activation.
    Lung cancer (Amsterdam, Netherlands) 05/2013; · 3.14 Impact Factor
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    ABSTRACT: Epidermal growth factor receptor (EGFR) mutation status is the most valuable indicator in the screening of non-small-cell lung cancer (NSCLC) patients for tyrosine kinase inhibitor (TKI) therapy. Accurate, rapid and economical methods of detecting EGFR mutations have become important. The use of two mutation-specific antibodies targeting the delE746-A750 mutation in exon 19 and L858R mutation in exon 21 makes this task possible, but the lack of consensually acceptable criteria for positive results limits the application of this antibody based mutation detection. We collected 399 specimens from NSCLC patients (145 resection specimens, 220 biopsy specimens, and 34 cytology specimens) whose EGFR mutation status had been detected by TaqMan PCR assay. Immunohistochemical (IHC) analyses using EGFR mutation-specific antibodies were employed for all samples. After staining and scoring, the sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) were calculated in accordance with different levels of positive grades in comparison with the results of PCR-based assay. In IHC-based analyses, 144 cases were scored 0, 104 cases were scored 1+, 103 cases were scored 2+, and 48 cases were scored 3+. With the molecular-based results were set as the "gold standard", the prevalence of mutation was 6.94% (10/144), 23.08% (24/104), 67.96% (70/103) and 100% (48/48), respectively, for samples with scores 0, 1+, 2+ and 3+. When score 3+ was considered positive, the specificity and PPV were 100%; if only score 0 was considered negative, 93.06% NPV was obtained. Patients with score 3+ have a perfect PPV (100%), and may accept TKI treatment directly without any molecular-based assays. Patients with score 0 had high NPV (93.06%), which could reach 97.22% when the detection of total EGFR was applied. However, samples with score 1+ or 2+ are unreliable and need further verification of EGFR mutation status by molecular-based assays.
    PLoS ONE 01/2013; 8(3):e59183. · 3.73 Impact Factor
  • Shuli Liu, Qianze Dong, Enhua Wang
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    ABSTRACT: Rsf-1 (HBXAP) was recently reported to be overexpressed in various cancers and associated with the malignant behavior of cancer cells. However, the expression of Rsf-1 and its biological roles in colon cancer have not been reported. The molecular mechanism of Rsf-1 in cancer aggressiveness remains ambiguous. In the present study, we analyzed the expression pattern of Rsf-1 in colon cancer tissues and found that Rsf-1 was overexpressed in 50.4 % of colon cancer specimens. There was a significant association between Rsf-1 overexpression and TNM stage (p = 0.0205), lymph node metastasis (p = 0.0025), and poor differentiation (p = 0.0235). Furthermore, Rsf-1 overexpression correlated with a poor prognosis in colon cancer patients (p = 0.0011). In addition, knockdown of Rsf-1 expression in HT29 and HCT116 cells with high endogenous Rsf-1 expression decrease cell proliferation and colony formation ability. Further analysis showed that Rsf-1 knockdown decreased cyclin E expression and phospho-Rb level. In conclusion, Rsf-1 is overexpressed in colon cancers and contributes to malignant cell growth by cyclin E and phospho-Rb modulation, which makes Rsf-1 a candidate therapeutic target in colon cancer.
    Tumor Biology 04/2012; 33(5):1485-91. · 2.52 Impact Factor
  • Qingchang Li, Qianze Dong, Enhua Wang
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    ABSTRACT: Rsf-1 (HBXAP) was recently reported to be overexpressed in various cancers and associated with the malignant behavior of cancer cells. However, the expression of Rsf-1 in primary lung cancer and its biological roles in non-small cell lung cancer (NSCLC) have not been reported. The molecular mechanism of Rsf-1 in cancer aggressiveness remains ambiguous. In the present study, we analyzed the expression pattern of Rsf-1 in NSCLC tissues and found that Rsf-1 was overexpressed at both the mRNA and protein levels. There was a significant association between Rsf-1 overexpression and TNM stage (p=0.0220) and poor differentiation (p=0.0013). Furthermore, knockdown of Rsf-1 expression in H1299 and H460 cells with high endogenous Rsf-1 expression resulted in a decrease of colony formation ability and inhibition of cell cycle progression. Rsf-1 knockdown also induced apoptosis in these cell lines. Further analysis showed that Rsf-1 knockdown decreased cyclin D1 expression and phospho-ERK levels. In conclusion, Rsf-1 is overexpressed in NSCLC and contributes to malignant cell growth by cyclin D1 and ERK modulation, which makes Rsf-1 a candidate therapeutic target in lung cancer.
    Biochemical and Biophysical Research Communications 02/2012; 420(1):6-10. · 2.41 Impact Factor
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    ABSTRACT: We aimed to investigate the clinical significance of the expression of novel scaffold protein CARMA3 in non-small-cell lung cancer (NSCLC) and the biological function of CARMA3 in NSCLC cell lines. We observed moderate to high CARMA3 staining in 68.8% of 141 NSCLC specimens compared to corresponding normal tissues. The overexpression of CARMA3 was significantly correlated with TNM stage (P = 0.022) and tumor status (P = 0.013). CARMA3 upregulation also correlated with a shorter survival rate of patients of nodal status N0 (P = 0.042)as well as the expression of epidermal growth factor receptor (EGFR) (P = 0.009). In EGFR mutation positive cases, CARMA3 expression was much higher (87.5%) compared to non-mutation cases (66.1%). In addition, we observed that knockdown of CARMA3 inhibits tumor cell proliferation and invasion, and induces cell cycle arrest at the boundary between the G1 and S phase. We further demonstrated a direct link between CARMA3 and NF-κB activation. The change of biological behavior in CARMA3 knockdown cells may be NF-κB-related. Our findings demonstrated, for the first time, that CARMA3 was overexpressed in NSCLC and correlated with lung cancer progression, EGFR expression, and EGFR mutation. CARMA3 could serve as a potential companion drug target, along with NF-kB and EGFR in EGFR-mutant lung cancers.
    PLoS ONE 01/2012; 7(5):e36903. · 3.73 Impact Factor
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    ABSTRACT: δ-Catenin (CTNND2), which encodes a scaffold protein in humans, has been found in a few malignancies. However, the expression pattern and contribution of δ-catenin to astrocytoma progression are unclear. We investigated δ-catenin expression in human astrocytoma samples and its function in astrocytoma cell lines using immunohistochemistry, siRNA knockdown, transfection, MTT, transwell migration and Rac1 pulldown techniques. δ-Catenin protein expression was detected in cytoplasm of astrocytoma cells by immunohistochemistry. Analysis showed that grade I astrocytoma (0%, 0/11) and glial cells from normal brain tissue exhibited negative staining. δ-Catenin expression was significantly higher in grade III-IV (35%, 29/84) compared to grade II astrocytoma cells (18%, 11/61); p < 0.01). In addition, CTNND2 overexpression promoted proliferation, invasion and Rac1 activity of U251 astrocytoma cells. Treatment of δ-catenin-transfected cells with a Rac1 inhibitor decreased Rac1 activity and invasion. δ-Catenin knockdown in U87 glioblastoma cell decreased cell proliferation, invasion and Rac1 activity. The results suggest that δ-catenin expression is associated with the malignant progression of astrocytoma and promotes astrocytoma cell invasion through upregulation of Rac1 activity. δ-Catenin expression levels may serve as a useful marker of the biological behavior of astrocytoma cells.
    BMC Cancer 12/2011; 11:514. · 3.33 Impact Factor
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    ABSTRACT: Downregulation of Mig-6 expression has been implicated in several human cancers and its loss can lead to prolonged activation of EGFR and carcinogenesis. The present study aimed to investigate the clinical significance of loss of Mig-6 expression in nonsmall-cell lung cancer (NSCLC) and the biological functions of Mig-6 in NSCLC cell lines. Mig-6 expression was downregulated in 47/91 (51.6%) cases of NSCLC that were examined. Mig-6 downregulation significantly correlated with poor differentiation (P = 0.0131), histological type (P = 0.0021), and EGFR expression (P = 0.003). In addition, knockdown of Mig-6 expression in H1299 and BE1 cells promoted EGF-induced tumor cell proliferation and migration. Furthermore, Mig-6 knockdown led to a significant increase in phospho-AKT, phospho-ERK, phospho-EGFR as well as MMP-2 and MMP-9 levels. These results indicate that downregulated Mig-6 in NSCLC tissues may serve as a new marker that can predict the activation of EGFR signaling pathway.
    Molecular Carcinogenesis 07/2011; 51(7):522-34. · 4.27 Impact Factor
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    ABSTRACT: Yes-associated protein (YAP), the nuclear effector of the Hippo pathway, is a key regulator of organ size and a candidate human oncogene. This study aimed to assess the clinical significance and biological functions of YAP in non-small-cell lung cancer (NSCLC). We investigated the expression of YAP in 92 cases of NSCLC tissue by immunohistochemistry and found that YAP was expressed in 66.3% (61/92) cases and predominantly presented in the nucleus. The expression of YAP in NSCLC was significantly correlated with p-TNM stage (P = 0.0037) and lymph node metastasis (P = 0.0093). Importantly, YAP expression was associated with short overall survival. Further study in NSCLC cell lines in which YAP was either overexpressed or depleted confirmed that YAP markedly promoted cell proliferation and invasion. These results indicate that YAP plays an important role in NSCLC and might be a useful therapeutic target of NSCLC.
    Cancer Science 01/2010; 101(5):1279-85. · 3.48 Impact Factor
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    ABSTRACT: p120(ctn) plays an important role in cell adhesion and has a significant association with tumorigenesis. To investigate the expression of p120(ctn) (p120 cateinin) isoforms in lung squamous cell carcinomas and adenocarcinomas, and analyze the correlation between p120(ctn) and clinicopathological parameters. The expression patterns of p120(ctn) in lung cancer tissues and the corresponding normal lung tissues were examined by reverse transcription-polymerase chain reaction (RT-PCR). Immunofluorescence, RT-PCR, and Western blot were used to investigate the expression of p120(ctn) isoforms in lung cancer cell lines BE1 and LH7. Compared with corresponding normal lung tissues, lung cancer tissues have significantly lower levels of total mRNA, isoform1 and 3 mRNA (P <0.001, P <0.001, P =0.001). Furthermore, reduction of p120(ctn) isoform 1 mRNA is negatively associated-whereas p120(ctn) isoform 3 is positively associated-with lymphatic metastasis (P =0.01, P =0.029). BE1 cells with 94% metastatic frequency has lower levels of p120(ctn) isoforms than LH7 cells with low metastatic potential. Reductions of p120(ctn) isoform 1 and 3 mRNA is a common phenomenon in lung cancer tissues and may play a role in metastasis progression of human lung cancer.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 08/2008; 11(4):529-33.