Ninghua Yao

Nantong University, Tungchow, Jiangsu Sheng, China

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Publications (7)13.82 Total impact

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    ABSTRACT: Overexpression of C-terminal binding protein-2 (CtBP2) has been noted to correlate with cancer metastasis in several human cancers including breast cancer. The aim of this study was to examine the effect of cyclase-associated protein 1 (CAP1) overexpression on CtBP2 expression and related mechanism in the metastasis of breast cancer. Immunohistochemical analysis was performed in 100 human breast carcinoma samples, and the data were correlated with clinicopathologic features. Furthermore, Western blot analysis was performed for CAP1 and CtBP2 in breast carcinoma samples and cell lines to evaluate their protein levels and molecular interaction. We found that the expression of CAP1 was positively related to CtBP2 expression (P < 0.01); moreover, CAP1 expression was significantly correlated with histologic grade (P < 0.01) and negatively related to E-cadherin expression (P < 0.01). Meanwhile, CtBP2 expression obtained similar results. Kaplan-Meier survival analysis showed that overexpression of CAP1 and CtBP2 exhibited a significant correlation with poor prognosis in human breast cancer (P < 0.01). While in vitro, we employed siRNA technique to knockdown CAP1 and CtBP2 expressions and observed their effects on MDA-MB-231 cells growth. CtBP2 depletion by siRNA-inhibited cell proliferation, resulted in increased E-cadherin levels. Moreover, knockdown of CAP1 resulted in decreased CtBP2 and increased E-cadherin expression. On the basis of these results, we suggested that CAP1's oncogenic abilities appear to be triggered at least in part by the modulation of CtBP2 and E-cadherin, which might serve as a future target for breast cancer.
    Medical Oncology 03/2014; 31(3):878. · 2.14 Impact Factor
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    ABSTRACT: Abnormal signaling of insulin-like growth factor I receptor (IGF-IR) is associated with hepatocellular carcinoma, but the underlying molecular mechanisms remain largely unknown. The objective of this study was to investigate IGF-IR's role as a signaling molecule, its pathological alteration in hepatoma tissues, and its effect on hepatoma cell proliferation when inhibited. As measured by immunohistochemical analysis, the incidence of hepatic IGF-IR expression in cancerous tissue was 80.0 % (24 of 30), which was significantly higher (P < 0.05) than 43.3 % (13 of 30) occurrence in the surrounding tissue and the nondetectable (0 of 30) frequency in the distal cancerous tissue. Hepatoma IGF-IR expression was correlated to the differentiation degree and not to the number or size of tumors, HBV infection, and AFP level. The in vitro IGF-IR expression in hepatoma cells was down-regulated significantly by picropodophyllin, a specific kinase inhibitor, in a time- and dose-dependent manner. Cell proliferation was inhibited through typical mechanisms of promoting apoptosis and cell cycle arrest (G2/M phase). Up-regulation of IGF-IR in hepatocarcinogenesis suggests that the down-regulation of IGF-IR expression could be a specific molecular target for hepatoma cell proliferation.
    Tumor Biology 06/2013; · 2.52 Impact Factor
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    ABSTRACT: Abnormal expression of insulin-like growth factor II (IGF-II) is associated with the hepatocyte malignant transformation and hepatocellular carcinoma (HCC) progress. In this study, specific IGF-II miRNA plasmids were constructed and transfected to HepG2 cells to knockdown IGF-II expression for observing effects on the cell proliferation, survival, apoptosis, angiogenesis, and anchorage-independent colony formation. IGF-II mRNA was evaluated by quantitative real-time polymerase chain reaction, and the level of IGF-II or vascular endothelial growth factor (VEGF) was quantitatively analyzed by ELISA. Our data shown that downregulation of IGF-II expression resulted in the viability alteration, proliferation inhibition, and apoptosis occurrence of HepG2 cells. The level of VEGF expression in the supernatant of HepG2 cells in the IGF-II-miRNA-transfected group was significantly decreasing (P < 0.01) than those in the untransfected group or the miRNA-neg-transfected group, with the susceptibility to anoikis and decreasing of anchorage-independent colony formation of HepG2 cells. Thus, we conclude that IGF-II is a potential molecular target for HCC gene therapy.
    Tumor Biology 06/2012; 33(5):1767-76. · 2.52 Impact Factor
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    ABSTRACT: Hypoxia-inducible factor-1 (HIF-1) is a ubiquitously expressed oxygen-regulated transcription factor composed of α and β subunits. HIF-1 activates the transcription of various genes including those involved in the formation and metastatic growth of hepatocellular carcinoma (HCC). To investigate the levels of hepatic and circulating HIF-1α expression in a range of patients with liver disease in order to determine how it can be used in the diagnosis of HCC and in establishing prognosis. Total RNA was extracted from a self-controlled HCC and paracancerous specimen. HIF-1α mRNA was amplified by nested RT-PCR and confirmed by sequencing. Tissue HIF-1α was analyzed by immunohistochemistry. The levels of HIF-1α, vascular endothelial growth factor (VEGF), and angiopoietin-2 (Ang-2) expression in the sera of 220 patients with liver disease were quantitatively detected by ELISA. The positive staining of liver HIF-1α was brown and granule-like and was mainly present in the cytoplasm, with lower levels in the nucleus of hepatocytes. Its incidence was 80% in HCC cells and 100% in paracancerous tissues, with no significant difference in HIF-1α expression in relation to tumor number, degree of differentiation, or hepatitis B surface antigen (HBsAg) positivity, but with some correlation between HIF-1α and tumor size. HIF-1α expression was detected in the sera of HCC patients at a significantly higher level than in cases of benign liver disease, with pathological characteristics associated with the levels of circulating VEGF and Ang-2 expression, the size of the tumor, and the level of extrahepatic metastasis, but not with patients' gender, age, or alpha-fetoprotein (AFP) levels. Hepatic HIF-1α expression is associated with the development and prognosis of HCC, and circulating HIF-1α level is a useful marker for HCC diagnosis and prognosis.
    Hepatitis Monthly 10/2011; 11(10):821-8. · 1.25 Impact Factor
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    ABSTRACT: Nuclear factor-kappaB (NF-κB) is a transcription factor and antagonist of apoptosis during liver regeneration and closely related to the formation and development of hepatocellular carcinoma. In the present study, we investigated the effect of small interference RNA (siRNA)-mediated inhibition of NF-κB on growth of human hepatoma (HepG2) cells. Our data indicated that the expression of NF-κB/p65 mRNA was significantly higher in the HepG2 cells than that in the normal liver (LO2) cells before transfection, and the expression of NF-κB/p65 in the HepG2 cells with NF-κB/p65 siRNA (100 nMol/L) transfection at 72 h was reduced at the levels of mRNA (93%) and protein (62%) using real-time reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay, and Western blotting. Interestingly, the apoptosis index of the HepG2 cells increased up to 85%, detected by Annexin V-fluorescein isothiocyanate, suggesting that NF-κB is overexpressed in hepatoma cells and can be inhibited by NF-κB/p65 siRNA through the apoptotic mechanism. Thus, we conclude that NF-κB is a potential molecular target for HCC gene therapy.
    Tumor Biology 12/2010; 31(6):605-11. · 2.52 Impact Factor
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    ABSTRACT: The prognosis of hepatocellular carcinoma (HCC) remains dismal. Insulin-like growth factor II (IGF-II), a fetal growth factor, is highly expressed during HCC development. We examined serum IGF-II levels and circulating IGF-II messenger RNA (mRNA) expression and analyzed the clinicopathologic characteristics in patients with liver diseases. The higher IGF-II level in the serum of patients with HCC could be correlated with hepatitis B virus infection but not with patient sex, age, tumor size, or α-fetoprotein (AFP) level. Total RNAs were extracted from liver tissues or peripheral blood mononuclear cells, and IGF-II complementary DNA (cDNA) and AFP cDNA were synthesized through random primers and reverse transcriptase; gene fragments were amplified by nested polymerase chain reaction and confirmed by sequencing. The incidence of the hepatic IGF-II gene was 100% in HCC, 54.3% in paracancerous tissues, and none in noncancerous tissues. The incidence rates for circulating IGF-II and AFP genes were 34.3% and 52.7%, respectively, and for both, 61.6% in patients with HCC. They were 100% in cases with extrahepatic metastasis. The IGF-II abnormality associates with HCC, and circulating IGF-II and IGF-II mRNA are useful molecular markers for HCC differential diagnosis and hematogenous metastasis.
    American Journal of Clinical Pathology 11/2010; 134(5):799-806. · 2.88 Impact Factor
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    ABSTRACT: Objective The aim of this study was to analyze the expression features of hypoxia inducible factor-1α (HIF-1α) in hepatocellular carcinoma (HCC) and effects of HIF-1α silencing on HepG2 cells. Methods HIF-1α expression was analyzed in the self-control HCC specimens by immunohistochemistry. After HepG2 cells with miRNA transfection, the expression of HIF-1α was determined at mRNA or protein level by real-time polymerase chain reaction (PCR) or Western blotting. Vascular endothelial growth factor (VEGF) and angiopoietin-2 (ANG-2) were determined by ELISA. Alterations of cell cycles and apoptosis of HepG2 cells were measured using a flow cytometer. Results Positive HIF-1α was brown and granule-like in the cytoplasm or nucleus. Significant difference was found between HCC (80%) and its surrounding tissues (100%, χ2 = 22.35, P < 0.001) and HIF-1α expression related to tumor size. At 72 h after miRNA transfection, the expression of HIF-1α in HepG2 cells was down-regulated by 87% at mRNA or 65% at protein level, with VEGF and ANG-2 decreased to 54% and 36%, respectively. After RNA interference combined with anti-cancer drug, the apoptotic rate of HepG2 cells was increasing from 22.46% ± 0.61% to 36.99% ± 0.88%, with up-regulation of G1 phase (65.68% ± 0.91%) and down-regulation of S phase (19.47 ± 1.34 %). Conclusion Abnormal expression of HIF-1α is associated with development of HCC, and HIF-1α gene silencing can effectively inhibit HepG2 cell proliferation.
    The Chinese-German Journal of Clinical Oncology 11(3).