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Cao Y.,Central Hospital of Zaozhuang Mining Group of Shandong Province | Chen Y.,Central Hospital of Zaozhuang Mining Group of Shandong Province | Huang Y.,Central Hospital of Zaozhuang Mining Group of Shandong Province | Liu Z.,No. 302 Hospital of PLA | Li G.,Weifang Medical University
Irish Journal of Medical Science | Year: 2016

Background: Aberrant promoter methylation of tumor suppressor gene can inhibit corresponding protein expression and promote carcinogenesis. Many studies have demonstrated that human mutL homolog 1(hMLH1) promoter methylation is correlated with occurrence and progression of multiple types of tumors. However, its correlation with esophageal carcinoma drug resistance is still unknown. Aims: To confirm methylation status of hMLH1 promoter in drug-resistance cell line of esophageal carcinoma, further confirm whether hMLH1 promoter methylation is responsible for drug resistance. Methods: Two stable esophageal carcinoma drug-resistance cell lines were successfully established by Cisplatin (DDP) concentration increment method; methylation status of hMLH1 promoter, mRNA and protein expression of hMLH1 were detected by methylation-specific PCR (MSP), RT-PCR and western blot, respectively; Drug-resistance ability assay was used to detect drug-resistance ability. Results: Stronger methylation status of hMLH1 promoter, lower hMLH1 mRNA and protein expression were found in both drug-resistance cell lines; after removing methylated bands using 5-aza-2′-deoxycytidine(5-Aza-CdR) in drug-resistance cell lines, hMLH1 mRNA and protein expression were restored and drug-resistance abilities declined nearly by half. Conclusion: hMLH1 promoter hypermethylation plays important roles in esophageal carcinoma drug-resistance and show us the prospect that combination of demethylation treatment with conventional chemotherapy drugs may bring better therapy effect. © 2016 Royal Academy of Medicine in Ireland Source


Cui H.,Beijing Institute of Radiation Medicine | Wu F.,Beijing Institute of Radiation Medicine | Sun Y.,No. 302 Hospital of PLA | Fan G.,Beijing Institute of Radiation Medicine | Wang Q.,Beijing Institute of Radiation Medicine
BMC Cancer | Year: 2010

Background: Hepatocellular carcinoma (HCC) is one of the world's leading causes of death among cancer patients. It is important to find a new biomarker that diagnoses HCC and monitors its treatment. In our previous work, we screened a single-chain antibody (scFv) N14, which could specifically recognize human HepG2 HCC cells but not human non-cancerous liver LO2 cells. However, the antigen it recognized in the cells remained unknown.Methods: Recombinant scFv N14 antibody was expressed as an active antibody. Using this antibody with a combination of immunological and proteomic approaches, we identified the antigen of scFv N14 antibody as the heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNP A2/B1). The expression of hnRNP A2/B1 in HCC cells was then investigated by semi-quantitative RT-PCR and immunohistochemistry.Results: We found that the up-regulation of hnRNP A2/B1 was measured at both transcriptional and translational levels in rat HCC cells but not in rat hepatic cells. We also found that in various human hepatic tissues, hnRNP A2/B1 was highly expressed in both human hepatitis virus positive liver tissues and human HCC tissues but not in normal liver tissues. Interestingly, we observed that the localization of hnRNP A2/B1 in HCC cells was altered during the development of HCC. In human hepatitis virus infected tissues hnRNP A2/B1 resides exclusively in the nuclei of hepatocytes. However, when the HCC progressed from a well differentiated to a poorly differentiated stage, hnRNP A2/B1 was increasingly localized in the cytoplasm. In contrast, the HCC tissues with hnRNP A2/B1 highly expressed in the nucleus decreased.Conclusions: This work is the first to show that hnRNP A2/B1 is the antigen specifically recognized by the scFv N14 antibody in HCC cells. The over-expression of hnRNP A2/B1 was confirmed in cultured human and rat HCC cell lines, human virus related hepatitis liver tissues and human HCC tissues. The increased localization of hnRNP A2/B1 in the cytoplasm of HCC cells was revealed during the dedifferentiation of hepatocellular carcinoma. Therefore, we suggest that the increased expression and cytoplasmic localization of hnRNP A2/B1 can be used as a diagnostic biomarker to assess the risk of human liver cancer. © 2010 Cui et al; licensee BioMed Central Ltd. Source


Liang G.,Chinese Academy of Sciences | Liang G.,Guiyang College of Traditional Chinese Medicine | Hu Z.,Chinese Academy of Sciences | Liu Q.,No. 302 Hospital of PLA | And 3 more authors.
Gaodeng Xuexiao Huaxue Xuebao/Chemical Journal of Chinese Universities | Year: 2014

N-(N-Benzoyl-L-phenylalanyl)-O-acetyl-L-phenylalanol was isolated from Dichondra repens Forst., which was a phenylalanine dipeptide compound with anti-HBV activity, named Matijin-Su (MTS). Its chemical skeleton structure was different from that of the existing drugs for anti-HBV. MTS was used as a lead compound base on the better anti-HBV activity by preliminary research. A series of MTS derivatives was designed and synthesized by a series of reactions, such as the formation of an amide (peptide), hydrolysis, condensation, acylation, alkylation and esterification using L-phenylalanine and its substitution as starting materials. The synthesized derivatives of MTS were characterized by 1H NMR, 13C NMR, ESI MS and elemental analysis. Their anti-hepatitis B virus activities against HepG2 2.2.15 cells line in vitro were tested. From the screening results, compounds 5b (IC50=8.20 μg/L, SI=10.26), 5g (IC50=5.58 μg/L, SI=22.78) and 5i (IC50=5.07 μg/L, SI=16.67) exhibited significant anti-HBV activities, the inhibition ratio were 56.57%, 67.06% and 66.83%, respectively. ©, 2014, Higher Education Press. All right reserved. Source


Wang H.,No. 302 Hospital of PLA | Liu G.-X.,No. 307 Hospital of PLA | Zhuo H.-L.,No. 307 Hospital of PLA | Bai W.-L.,No. 302 Hospital of PLA | And 6 more authors.
Chinese Journal of Cancer Biotherapy | Year: 2010

Objective: To observe the efficacy of endothelial progenitor cells carrying hIFN-γ (EPCs-hIFN-γ) in cancer maintenance therapy after chemotherapy. Methods: MTT was used to examine the inhibitory effects of hIFN-γ and/or C225 against colorectal cancer LoVo cells after treatment with CPT-11. The in vivo inhibitory effects of EPCs-hIFN-γ and/or C225 on LoVo tumors and their effects on survival of LoVo tumor-bearing nude mice were investigated after mice had been treated with CPT-11. Results: In vitro, hIFN-γ and/or C225 further inhibited the growth of cancer cells after CFT-11 treatment. In vivo, after 50 mg/kg CPT-11 treatment, EPCs-hIFN-γ, C225 and EPCs-hIFN-γ + C225 inhibited the growth of tumors in LoVo tumor-bearing nude mice (mean tumor volumes: [2024.28 ± 1048.40] mm 3 vs [764.94 ± 720.14], [233.85 ± 186.97], [186.95 ± 133.43], [163.9 ± 173.39] mm3; P < 0.05). EPCs-hIFN-γ, C225 and EPCs-hIFN-γ + C225 treatment also increased the survival of tumor-bearing mice (median survival: 34.2 d vs 39.4, 44.5, 48.5, 51.3 d; P < 0.05 or P < 0.01). Conclusion: EPC-hIFN-γ can inhibit the tumor growth and prolong the survival of tumor-bearing mice in cancer maintenance therapy after chemotherapy. Source


Song C.,No. 302 Hospital of PLA | Chen L.,No. 302 Hospital of PLA | Yang B.,No. 302 Hospital of PLA | Chi S.,No. 302 Hospital of PLA | Cheng Y.,No. 302 Hospital of PLA
Journal of Medical Colleges of PLA | Year: 2010

Objective: To investigate the actions of cytokine profile in the immune cells by a seven amino acid peptide mimic from HVR1 of HCV (GQTYTSG, named 7P). Methods: The peripheral blood mononuclear cells (PBMCs) from 17 healthy blood donors were stimulated with 7P, and the cytokine levels in CD4 +CD8-,CD4-CD8+ T cells, NK, NKT cells were analyzed by the intracellular cytokine staining. Results: The frequency of cells which secreted interferon-γ (IFN-γ) was found to be significantly increased in all cells, interleukin-10(IL-10) was significantly increased in CD4+CD8-, CD4- CD8+ T cells but decreased in NK, NKT cells, and tumor necrosis factor-α (TNF-α) was decreased in CD4+CD8-, CD4- CD8+ but increased in NK cells. Conclusion: 7P could induce a cytokine profile in different immune cells in vitro and there was some difference between the CD4+CD8-,CD4- CD8 + T cells which represented the adaptive immunity cells and NK, NKT cells which represented the innate immunity cells.This kind of variation of cytokine profile might contribute to anti-virus and anti-inflammatory immune reaction. Source

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