Bing Li

The Third Xiangya Hospital of the Central South University, Ch’ang-sha-shih, Hunan, China

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Publications (8)12.88 Total impact

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    ABSTRACT: Objective: To determine the effect of transforming growth factor-β1 (TGF-β1) on the expression of telomerase in hepatic stellate cells (HSCs) in rats and the role of TGF-β1 in the development of liver fibrosis. Methods: Primary HSCs were isolated from normal rats by density gradient separation and divided into 2 groups for culturing. The morphology of HSCs was identified by the inverted fluorescence microscope. The purity of HSCs was identified by immunohistological expression and fluorescence analysis. One group of HSCs was treated with different concentrations (0, 0.1, 1, and 10 ng/mL) of TGF-β1 for 24 h, while the other group was treated with 1 ng/mL TGF-β1 and cultured for 3, 6, and 9 days. The mRNA expression of telomerase reverse transcriptase (TERT) was assessed and compared by polymerase chain reaction. Results: Cell morphology showed that TGF-β1 triggered the differentiation of HSCs from a quiescent phenotype into highly activated myofibroblasts. TERT mRNA expression in the primary HSCs showed slight increase with the culture time, though with no statistical difference between the results at various time points (P>0.05). TGF-β1 at 0.1 ng/mL did not significantly affect the TERT mRNA level compared with the 0 ng/mL group, while 1 ng/mL and 10 ng/mL TGF-β1 significantly decreased the level of TERT mRNA (P<0.05). TGF-β1 at 1 ng/mL had only weak effect on TERT mRNA expression after the 3 day treatment compared with the 0 ng/mL group (P>0.05). TGF-β1 at 1 ng/mL significantly inhibited TERT mRNA expression 6 days after the treatment (P<0.05). TGF-β1 inhibited the expression of TERT mRNA level in the HSCs in both dose- and time-dependent manner. Conclusion: TGF-β1 may contribute to the transdifferentiation of HSCs by reducing TERT levels to develop hepatic fibrosis.
    No preview · Article · May 2014 · Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
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    ABSTRACT: Objective: To conduct a meta-analysis to determine the efficacy of peginterferon alpha (PEG-IFN α) therapy versus IFN α, adefovir dipivoxil (ADV) and entecavir (ETV) for HBeAg-positive chronic hepatitis B patients in China. Methods: MEDLINE database and 3 main Chinese biomedical databases between 1966 and 2012 was retrieved. Two reviewers independently screened all reports to identify randomized controlled trials that evaluated PEG-IFN α therapy for the treatment of chronic hepatitis B in China. Results: Fourteen trials met the eligibility criteria for this Meta analysis. PEG-IFN α therapy was more effective than IFN α therapy in achieving ALT normalization, serum HBV DNA clearance, HBeAg seroconversion, serum HBeAg clearance and fibrosis improvement in Chinese hepatitis B patients (P<0.05). PEG-IFN α was obviously superior to ETV in HBeAg seroconversion and serum HBeAg clearance (P<0.05), but the seroconversion rate was low. The combination therapy of PEG-IFN α and ADV was more effective than ADV monotherapy in ALT normalization, serum HBV DNA clearance and HBeAg seroconversion (P<0.05). PEG-IFN α showed no priority to other treatment regimes in HBsAg clearance. Conclusion: Treatment with PEG-IFN α is safe and effective, and can be prescribed as firstline treatment options for chronic hepatitis B patients in China. Data are too limited to exclude a substantial benefit or harm of PEG-IFN α combination therapy for CHB patients in China.
    No preview · Article · Dec 2013 · Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
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    ABSTRACT: Raf kinase inhibitory protein (RKIP) is an inhibitor of the Raf/MEK/MAP kinase signaling cascade and a suppressor of cancer metastasis. But its function in pancreatic cancer was not yet clarified completely. The aim of this study was to investigate the involvement of RKIP in pancreatic cancer. RKIP expression was investigated retrospectively by immunohistochemistry in paraffin-embedded primary tumor tissue samples from a series (n = 99) of consecutive patients with pancreatic cancer. Survival was calculated using Kaplan-Meier curves. Parameters found to be of prognostic significance in univariate analysis were verified in a multivariate Cox regression model. RKIP expression was high in normal pancreatic epithelium and retained to varying degrees in pancreatic cancer tissues. However, in tumor tissues with lymph node metastasis (P = 0.008) and high UICC stage (P = 0.006), RKIP expression was highly significantly reduced or lost. Furthermore, the reduced expression of RKIP significantly correlated with both poor overall and disease-free survival (P = 0.008 and 0.01, respectively). Multivariate analyses revealed RKIP to be an independent prognosticator. These findings suggest that RKIP could be a promising marker for predicting a better prognosis in pancreatic cancer.
    No preview · Article · Jul 2012 · Clinical and Translational Oncology
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    ABSTRACT: Lung adenocarcinoma is the most frequently histologic subtype and the most histologically heterogeneous form of lung cancer. De-regulation of Wnt/β-catenin signaling pathway is implicated in lung carcinogenesis. SOX7, as a member of high mobility group (HMG) transcription factor family, plays a role in the modulation of the Wnt/β-catenin signaling pathway. However, the expression pattern and clinicopathological significance of SOX7 in patients with lung adenocarcinoma is still unclear. To address this problem, the SOX7 mRNA expression was detected by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). Immunohistochemical studies were performed on 288 pairs of adjacent normal lung and lung adenocarcinoma tissues with complete follow-up records. Association of SOX7 protein expression with clinical outcomes was evaluated using the Kaplan-Meier method and a multivariate Cox proportional hazards regression model. SOX7 mRNA expression was significantly down-regulated in lung adenocarcinoma compared with matched adjacent normal tissues (P < 0.001). SOX7 protein was expressed in the cytoplasm of lung adenocarcinoma cells in 106/288 (36.8 %) of cases, whereas its immunoreactivities were predominantly located in the cytoplasm of the adjacent normal tissues. The reduced SOX7 expression was correlated with poor differentiation (P = 0.002), lymph node metastasis (P = 0.011) and advanced TNM stage (P = 0.006). Regarding patient survival, the overall survival and the disease-free survival rates were both significantly lower in patients with SOX7-negative tumors than in those with SOX7-positive tumors (P = 0.018 and 0.013, respectively). Multivariate analysis using a Cox proportional-hazards model demonstrated that SOX7 expression status was an independent prognostic factor predicting the overall survival and the disease-free survival of patients with lung adenocarcinoma (P = 0.021 and 0.016, respectively).Our data suggest that the decreased expression of SOX7 is an important feature of lung adenocarcinoma. The expression level of SOX protein may be a useful prognostic marker for patients with lung adenocarcinoma.
    No preview · Article · Jul 2012 · Pathology & Oncology Research
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    ABSTRACT: To investigate the clinicopathological and prognostic value of a disintegrin and metalloprotease 8 (ADAM8) in osteosarcoma. ADAM8 expression in osteosarcoma tissues was examined by immunohistochemistry in 69 patients. ADAM8 was positively expressed in 61 of 69 (88.4%) osteosarcoma specimens with cytoplasmic staining, and also increased in the specimens with recurrence (P = 0.008) and metastasis (P = 0.002). Patients with strong ADAM8 expression had significantly poorer overall survival (OS) and disease-free survival (DFS) (both P < 0.001) when compared with the patients with the weak expression of ADAM8. On multivariate analysis, ADAM8 expression was found to be an independent prognostic factor for both OS (P < 0.001) and DFS (P < 0.001). Our results suggest for the first time that ADAM8 might be applied as a novel marker for the prediction of recurrence and metastasis potency and a significant indicator of poor prognosis for patients with osteosarcoma.
    No preview · Article · Jan 2012 · Pathology & Oncology Research
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    ABSTRACT: Nuclear factor-kappa B (NF-kappaB) regulates the expression of various genes, several genes involved in inflammation and tumorigenesis, including those of the liver. A role for NF-kappaB has been implicated in the pathogenesis of hepatocellular carcinoma. This transcription factor can regulate hTERT gene transcription. Expression of hTERT was found to be at high levels in hepatocellular carcinoma. However, positive effects of NF-kappaB on hTERT protein synthesis in HepG(2) cells are unknown. In this study, we show that LPS (specific binding to TLR4 to activate NF-kappaB) was positive for NF-kappaB p65 mRNA expression and activation, and also up-regulated hTERT mRNA and protein expressions at 36h in a dose-dependent manner. In contrast, MG-132 (blocking the activity of 26S proteasome and thereby preventing nuclear translocation of NF-kappaB) significantly inhibited activation of NF-kappaB and mRNA expression. And also reduced the expression of hTERT at both mRNA and protein levels at 36h in a dose-dependent manner. Furthermore, dexamethasone inhibited LPS-induced activation of NF-kappaB and expression of the hTERT in HepG(2) cells. These findings suggest that NF-kappaB may modulate hTERT mRNA level, importantly, in protein level in HepG(2) cells and dexamethasone inhibits LPS-induced hTERT via blocking NF-kappaB.
    No preview · Article · Dec 2011 · European journal of pharmacology
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    ABSTRACT: N-myc downstream-regulated gene 1 (NDRG1), a member of the N-myc downstream-regulated gene family, is induced under a wide variety of stress and cell growth-regulatory conditions. In several cancers, recent studies have shown its association with inhibition of tumor metastasis and suggested it to be a tumor suppressor gene. However, its significance in primary gallbladder carcinoma (PGC) has not been studied. Therefore, the aim of this study was to investigate NDRG1 expression in PGC and its prognostic significance. We examined NDRG1 expression in tumor specimens from 138 patients with PGC by immunohistochemistry and analyzed the correlation between NDRG1 expression and clinicopathologic factors or survival. NDRG1 was expressed in 63.8% of PGC but not in the normal epithelium of the gallbladder, remarkably at the invasive front of the tumors. In addition, NDRG1 expression was significantly associated with high histologic grade, advanced pathologic T stage and clinical stage, positive nodal metastasis and venous/lymphatic invasion. Moreover, Kaplan-Meier curves showed that NDRG1 over-expression was significantly related to poor overall and disease-free survival (both P = 0.02). Furthermore, multivariate analyses showed that NDRG1 expression (hazard ratio, 3.338; P = 0.02) and clinical stage (hazard ratio, 3.128; P = 0.03) were independent risk factors for disease-free survival. Our data demonstrate for the first time that NDRG1 expression in PGC was significantly correlated with unfavorable clinicopathologic features and an independent poor prognostic factor for disease-free survival in patients. Taken together, our findings suggest that NDRG1 expression could be used as a novel prognostic factor for patient survival and might be a potential therapeutic target in PGC.
    No preview · Article · Jul 2011 · Medical Oncology
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    ABSTRACT: Probe 1 was designed and synthesized as a new fluorescent molecular probe for thiols in PBS buffer at physiological condition. This fluorescent molecular probe consists of a thiol reaction moiety bound to a coumarin fluorophore. Its fluorescence quantum yield is low, but a drastic enhancement of fluorescence intensity was observed in the presence of thiols. Possible interference with other analytes was examined. Probe 1 displays a highly selective fluorescent enhancement with thiols, and the probe was successfully applied to thiols determination in intracellular, in human urine and blood samples.
    No preview · Article · Nov 2010 · Journal of Fluorescence