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Zheng J.,General Hospital of Guangzhou Military Command | Zhou J.,General Hospital of Guangzhou Military Command | Xie X.,Northwest University, China | Xie X.,Institute of Integrated Medical Information | And 4 more authors.
DNA and Cell Biology | Year: 2014

Few studies have referred to the implication of anoikis processes following hormonal treatment. No data are available on the influence of estrogen in ovarian cancer anoikis. To gain insights into the effects and mechanism of estrogen in ovarian cancer cells, we have carried out studies on the anoikis of ovarian cancer cells treated with estrogen and on the pathways involved. We observed an anti-anoikis role of E2 in suspended Caov-3 cells, and this was mainly due to the decreasing of Bit1 level in cytosol. We also found that estrogen receptor α (ERα) was the main mediator involved in this process. To study the signaling pathways well, phosphatidylinositol 3-kinase (PI3K)/AKT were further investigated. Results demonstrated that the decreasing of the Bit1 level in cytosol mediated by E2 binding to ERα was mainly through PI3K/AKT pathways. Overall, these findings disclose a new perspective for estrogen on ovarian cancer therapy. © Mary Ann Liebert, Inc. 2014.


Bai J.,Xian Jiaotong University | Xie X.,Northwest University, China | Xie X.,Institute of Integrated Medical Information | Lei Y.,Xian Jiaotong University | And 3 more authors.
Molecular Medicine Reports | Year: 2014

Malignant melanoma has the highest risk of mortality among all types of skin cancer due to its highly metastatic potential. The ocular albinism type 1 (OA1) protein is a pigment cell-specific glycoprotein, which shares significant structural and functional features with G protein-coupled receptors. However, the role of OA1 in melanoma has yet to be elucidated. The present study aimed to investigate whether OA1 is involved in melanoma cell migration. OA1 was found to stimulate cell migration in a dose-dependent manner in cultured human melanoma cells. Furthermore, knockdown of OA1 using small interfering RNA was observed to significantly inhibit melanoma cell migration. In addition, the mechanism underlying OA1-induced melanoma cell migration was investigated. Stimulation of the RAS/RAF/mitogen activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway using growth factors enhanced OA1 expression and melanoma cell migration, whereas inhibition of this pathway using U0126 was observed to markedly decrease OA1 expression and the number of migrated cells. These findings indicate that OA1 is involved in melanoma cell migration and that OA1-induced melanoma cell migration is mediated through the RAS/RAF/MEK/ERK signaling pathway. Therefore, OA1 may serve as a novel therapeutic target for melanoma.


Guo C.,Xian Jiaotong University | Guo C.,Key Laboratory of Infection and Immunity Disease of Shaanxi Province | Xie X.,Northwest University, China | Xie X.,Institute of Integrated Medical Information | And 18 more authors.
Experimental and Molecular Pathology | Year: 2015

Influenza A virus infection is a persistent threat to public health worldwide due to hemagglutinin (HA) variation. Current vaccines against influenza A virus provide immunity to viral isolates similar to vaccine strains. Antibodies against common epitopes provide immunity to diverse influenza virus strains and protect against future pandemic influenza. Therefore, it is vital to analyze common HA antigenic epitopes of influenza virus. In this study, 14 strains of monoclonal antibodies with high sensitivity to common epitopes of influenza virus antigens identified in our previous study were selected as the tool to predict common HA epitopes. The common HA antigenic epitopes were divided into four categories by ELISA blocking experiments, and separately, into three categories according to the preliminary results of computer simulation. Comparison between the results of computer simulations and ELISA blocking experiments indicated that at least two classes of common epitopes are present in influenza virus HA. This study provides experimental data for improving the prediction of HA epitopes of influenza virus (H1 subtype) and the development of a potential universal vaccine as well as a novel approach for the prediction of epitopes on other pathogenic microorganisms. © 2014 Elsevier Inc.


Xie X.,Northwest University, China | Xie X.,Institute of Integrated Medical Information | Wu X.,Shanghai Tenth Peoples Hospital | Cui J.,Northwest University, China | And 2 more authors.
Brain Research | Year: 2013

Subarachnoid hemorrhage (SAH) is a frequent occurrence in cerebrovascular accidents, and inflammation occurs in the subarachnoid space after SAH. Arachnoid cells have the capability to present antigens and active T-lymphocytes after stimulation by cerebrospinal fluid (CSF). However, the effect of CSF on T-lymphocytes and arachnoid cell adhesion was not clearly understood. In this study, we used ELISA to detected tumor necrosis factor-α (TNF-α) content in CSF of SAH patients. CSF or recombinant TNF-α were applied on arachnoid cells and T-lymphoctes, and RT-PCR and western blotting were performed to determine the expression of intercellular adhesion molecule-1 (ICAM-1) in arachnoid cells and Lymphocyte Function-Associated Antigen-1 (LFA-1) in T-lymphocytes, respectively. Meanwhile, the Matrix Metal Proteinase-9 (MMP-9) expression in these cells was also determined. We found that the content of TNF-α in the CSF was significantly increased in the CSF of SAH patients (from 22±8 pg/mL of healthy people to 436-450 pg/mL of SAH patients). Treatement with CSF could increase the expression of ICAM-1in arachnoid cells and that of LFA-1 in T-lymphocytes, mainly through the increased levels of TNF-α. We also found that the co-culture of arachnoid cells and T-lymphocytes increased the expression of MMP-9 in both cells through the interaction of ICAM-1 of and LFA-1. All of these results suggested that arachnoid cells are involved in the T-lymphocytes invasion in the subarachnoid space after SAH. © 2013 Elsevier B.V.


Hao H.,Northwest University, China | Zhen Y.,Northwest University, China | Wang Z.,Peking University | Chen F.,Northwest University, China | And 2 more authors.
Cell Biology International | Year: 2013

Colon cancer is a type of malignant tumor that causes considerable mortality worldwide. Epithelial cellular adhesion molecule (EpCAM), a tumor-associated antigen of colon tumors, is a target for colon cancer therapy. EpCAM-specific monoclonal antibodies (mAbs) have been applied in human colon cancer since the 1990s; however, the therapeutic effects are limited. EpCAM activates nuclear signaling pathways by releasing its intracellular domain (EpICD). The released EpICD stimulates the Wnt/b-catenin signaling pathway, which is also strongly associated with tumorigenesis. EpCAM is also a target gene of the Wnt/ b-catenin signaling pathway. EpCAM and the Wnt/b-catenin signaling pathway form a functional interaction cycle in colon cancer. Thus, we propose a new therapeutic drug for colon cancer: an EpCAM single-chain fragment variable antibody (scFv)- truncated protamine-siRNA. EpCAM scFv can recognize and bind colon cancer cells through its EpCAM antigen activity. Furthermore, the specific siRNA transferred into colon cancer cells specifically inhibits Wnt/b-catenin signal transmission. Therefore, this new drug may efficiently interrupt the functional cycle between EpCAM and Wnt/b-catenin signaling and be an effective therapeutic strategy for colon cancer. © 2013 International Federation for Cell Biology.

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