Junfen Ma

Zhengzhou University, Cheng, Henan Sheng, China

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Publications (6)14.74 Total impact

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    ABSTRACT: Esophageal cancer is an intractable disease due to late diagnosis, high incidence of post-surgical locoregional recurrence and frequent distant metastasis. Oncolytic adenovirus (Ad) vectors are a promising method for cancer treatment. The H101 virus is a recombinant Ad which has replication-selective properties and replicates only in tumor cells. The coxsackievirus and adenovirus receptor (CAR) is considered a surrogate marker that monitors the outcome of Ad-mediated gene therapy. Accumulating evidence indicates that CAR expression levels are lower in various types of tumors such as ovarian, lung, breast and bladder when compared to their normal counterparts. In this study, we reported that trichostatin A (TSA) induced the expression of CAR in esophageal squamous cell carcinoma (ESCC) cell lines through the MAPK/ERK1/2 signaling pathway. The expression levels of CAR were positively related with the antitumor activity of H101. Our results suggest that TSA increases the antitumor activity of the oncolytic adenovirus H101 through the MAPK/ERK pathway.
    International Journal of Molecular Medicine 09/2012; · 1.96 Impact Factor
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    ABSTRACT: Alternariol (AOH) is a mycotoxin of Alternaria alternata and can cause DNA damage and gene mutations. Low-dose and long-term treatment with AOH has been linked with incidence of esophageal carcinoma. DNA polymerase β (polβ) is a key enzyme in DNA base excision repair (BER). When it is overexpressed or mutated in cells, DNA polβ can cause genetic instability. Elevated DNA polβ has also been reported in several human cancers. Here, we report that AOH at 2, 10, 20 µM induces DNA polβ expression. In the process, protein kinase A (PKA) catalytic subunit activation, nuclear translocation and cAMP response element binding protein (CREB) phosphorylation are involved. AOH also increased CREB binding to the cAMP response element (CRE) consensus motif, which is present in the DNA polβ gene promoter. The PKA inhibitor H89 was able to block AOH-induced PKA-CREB activation, CREB DNA binding activity and decrease DNA polβ expression. Our results suggest that AOH can upregulate DNA polβ expression through the PKA-CREB signal transduction pathway.
    International Journal of Oncology 03/2012; 40(6):1923-8. · 2.66 Impact Factor
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    ABSTRACT: Dendritic cells (DCs) are professional antigen-presenting cells that play an important role in anti-tumour immunity. Endothelial-like differentiation of DCs is an interesting phenomenon. The specific role of vascular endothelial growth factor-A (VEGF-A) on the differentiation of immature DCs (iDCs) and mature DCs (mDCs) is worth further research. Here, we show that VEGF-A can induce iDCs to differentiate into endothelial-like cells (ELCs). But it has no obvious influence on mDCs. In the process of endothelial-like differentiation of iDCs, a sustained activation of extracellular signal-regulated kinase (ERK1/2) and cAMP response element binding protein (CREB) was detected. VEGF-A induced the activation of ERK1/2, and led to the nuclear translocation of phosphorylation ERK1/2. Incubation of iDCs with the ERK1/2 upstream kinase MEK1/2 inhibitor PD98059, blocked the phosphorylation of ERK1/2 and CREB as well as the endothelial-like differentiation of iDCs. These data suggest that VEGF-A induces endothelial-like differentiation of iDCs not mDCs through ERK1/2 signalling pathway.
    Cell Biochemistry and Function 06/2011; 29(4):294-302. · 1.85 Impact Factor
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    ABSTRACT: Endothelial-like differentiation of dendritic cells (DCs) is an interesting and significant phenomenon, which is worth further investigation. Here, we show that the tumor microenvironment derived from the supernatant of the SW620 human colon adenocarcinoma cell line and colon adenocarcinoma tissue homogenate can promote immature DCs (iDCs) to differentiate from the DC pathway toward endothelial cells, while the peri-carcinoma homogenate supernatant does not have this role. Inhibition of angiopoietin-2 (Ang2) in the supernatant by its antibody has no obvious influence on the endothelial-like differentiation. In contrast, inhibition of vascular endothelial growth factor-A (VEGF-A) blocked the differentiation. During the course of differentiation, a sustained activation of ERK1/2 was detected. PD98059 blocked the phosphorylation of ERK1/2 as well as the endothelial-like differentiation of iDCs. Inhibition of VEGF-A also blocked the phosphorylation of ERK1/2. These data suggest that VEGF-A not Ang2 mediates endothelial-like differentiation of iDCs by ERK1/2 signaling in the microenvironment of human colon adenocarcinoma.
    International Journal of Oncology 03/2011; 38(6):1579-88. · 2.66 Impact Factor
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    ABSTRACT: Endothelial-like differentiation of dendritic cells (DCs) is a new phenomenon, and the mechanism is still elusive. Here, we show that the tumor microenvironment derived from the human esophageal squamous cell carcinoma (ESCC) cell line EC9706 can induce immature DCs (iDCs) differentiate toward endothelial cells, and become endothelial-like cells, but it has no obvious influence on mature DCs. During the course of endothelial-like differentiation of iDCs, a sustained activation of mitogen-activated protein kinase/extracelluar signal-regulated kinase1/2 (MAPK/ERK1/2) and cAMP response element-binding protein (CREB) was detected. Incubation of iDCs with MEK phosphorylation inhibitor PD98059 blocked the MAPK/ERK1/2 and CREB phosphorylation as well as the endothelial-like differentiation of iDCs. Inhibition of vascular endothelial growth factor-A (VEGF-A) in the microenvironment with its antibody blocked the endothelial-like differentiation and the phosphorylation of MAPK/ERK1/2 and CREB. These data suggest that MAPK/ERK1/2 signaling pathway activated by VEGF-A could mediate endothelial-like differentiation of iDCs in the ESCC microenvironment.
    Cellular and Molecular Life Sciences CMLS 03/2010; 67(12):2091-106. · 5.62 Impact Factor
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    ABSTRACT: To study the cytotoxicity of altemariol (AOH) on NIH/3T3 cells. Logarithmic growth phase NIH/3T3 cells were treated at the dose of 10 micromol/L and 50 micromol/L AOH as treatment groups and treated with DMSO (0.25%). The effects of AOH on cell proliferations were assessed by morphologic observasion. Inhibition rates of AOH were determined by MTT assay. Comet assay was used to examine DNA damage induced by AOH. Cell cycle distributions were detected by flow cytometric assay (FCM). The cells treated with AOH occured morlogic changes. The inhibition rates of 10 micromol/L and 50 micromol/L AOH were 19.88% and 32.47% respectively. In the comet assay two treatment groups percentages of tailed cells were 35.87% and 71.83% respectively. The DNA contents of the tail were (36.18 +/- 18.6) and (51.3 +/- 21.6) respectively. These datas were more higher than those of the solvent control (P < 0.05). In comparison with the control group, the percents of G2/M and S phase cells were increased after treatment of 50.0 micromol/L AOH for 24h (P < 0.05). AOH could have acute cytotoxic effects on NIH/3T3 cells and inhibite cell proliferation and cause DNA damage. High dose of AOH could induce cell cycle arrest in G2/M phase.
    Wei sheng yan jiu = Journal of hygiene research 03/2009; 38(2):133-5.