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Articles by W Xie
Total Records ( 5 ) for W Xie
  J Meng , W Xie , L Cao , C Hu and Z. Zhen
 

Hepatoma-derived growth factor (HDGF), a nuclear protein with both mitogenic and angiogenic activity, has been reported to be mainly involved in tumorigenesis and the progression of non-small cell lung cancer. In this study, the HDGF expression was knocked down by specific-shRNA with lentivirus expression vector targeting HDGF in lung squamous cell carcinoma 520 cells. HDGF knocked down by shRNA suppressed the cell proliferation significantly both in vitro and in vivo as indicated by MTT, plate clone and transplanted tumor model assays. In addition, the knocked-down expression of HDGF also inhibited cell migration and invasion as shown in transwell and Boyden experiments. We concluded that HDGF acts as an oncogene participating in the pathogenesis of squamous cell lung cancer, and HDGF may be a key therapeutic target for non-small cell lung cancer.

  J Ding , G He , W Gong , W Wen , W Sun , B Ning , S Huang , K Wu , C Huang , M Wu , W Xie and H. Wang
 

Frequent exposure to nickel compounds has been considered as one of the potential causes of human lung cancer. However, the molecular mechanism of nickel-induced lung carcinogenesis remains obscure. In the current study, slight S-phase increase, significant G2/M cell cycle arrest, and proliferation blockage were observed in human bronchial epithelial cells (Beas-2B) upon nickel exposure. Moreover, the induction of cyclin D1 and cyclin E by nickel was shown for the first time in human pulmonary cells, which may be involved in nickel-triggered G1/S transition and cell transformation. In addition, we verified that hypoxia-inducible factor-1, an important transcription factor of nickel response, was not required for the cyclin D1 or cyclin E induction. The role of p53 in nickel-induced G2/M arrest was excluded, respecting that its protein level, ser15 phosphorylation, and transcriptional activity were not changed in nickel response. Further study revealed that cyclin A was not activated in nickel response, and cyclin B1, which not only promotes G2/M transition but also prevents M-phase exit of cells if not degraded in time, was up-regulated by nickel through a manner independent of hypoxia-inducible factor. More importantly, our results verified that overexpressed cyclin B1, veiling the effect of cyclin D1 or cyclin E, mediated nickel-caused M-phase blockage and cell growth inhibition, which may render pulmonary cells more sensitive to DNA damage and facilitates cancer initiation. These results will not only deepen our understanding of the molecular mechanism involved in nickel carcinogenecity, but also lead to the further study on chemoprevention of nickel-associated human cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1720–9)

  X Wang , W Xie , Y Zhang , P Lin , L Han , P Han , Y Wang , Z Chen , G Ji , M Zheng , N Weisleder , R. P Xiao , H Takeshima , J Ma and H. Cheng
 

Rationale: Unrepaired cardiomyocyte membrane injury causes irreplaceable cell loss, leading to myocardial fibrosis and eventually heart failure. However, the cellular and molecular mechanisms of cardiac membrane repair are largely unknown. MG53, a newly identified striated muscle-specific protein, is involved in skeletal muscle membrane repair. But the role of MG53 in the heart has not been determined.

Objective: We sought to investigate whether MG53 mediates membrane repair in cardiomyocytes and, if so, the cellular and molecular mechanism underlying MG53-mediated membrane repair in cardiomyocytes. Moreover, we determined possible cardioprotective effect of MG53-mediated membrane repair.

Methods and Results: We demonstrated that MG53 is crucial to the emergency membrane repair response in cardiomyocytes and protects the heart from stress-induced loss of cardiomyocytes. Disruption of the sarcolemmal membrane by mechanical, electric, chemical, or metabolic insults caused rapid and robust translocation of MG53 toward the injury sites. Ablation of MG53 prevented sarcolemmal resealing after infrared laser–induced membrane damage in intact heart, and exacerbated mitochondrial dysfunction and loss of cardiomyocytes during ischemia/reperfusion injury. Unexpectedly, the MG53-mediated cardiac membrane repair was mediated by a cholesterol-dependent mechanism: depletion of membrane cholesterol abolished, and its recovery restored injury-induced membrane translocation of MG53. The redox status of MG53 did not affect initiation of MG53 translocation, whereas MG53 oxidation conferred stability to the membrane repair patch.

Conclusions: Thus, cholesterol-dependent MG53-mediated membrane repair is a vital, heretofore unappreciated cardioprotective mechanism against a multitude of insults and may bear important therapeutic implications.

  L Jin , D Martynowski , S Zheng , T Wada , W Xie and Y. Li
 

The retinoic acid-related orphan receptor (ROR) has important roles in development and metabolic homeostasis. Although the biological functions of ROR have been studied extensively, no ligands for ROR have been identified, and no structure of ROR has been reported. In this study, we showed that hydroxycholesterols promote the recruitment of coactivators by ROR using biochemical assays. We also report the crystal structures of the ROR ligand-binding domain bound with hydroxycholesterols. The structures reveal the binding modes of various hydroxycholesterols in the ROR pocket, with the receptors all adopting the canonical active conformation. Mutations that disrupt the binding of hydroxycholesterols abolish the constitutive activity of ROR. Our observations suggest an important role for the endogenous hydroxycholesterols in modulating ROR-dependent biological processes.

  K Kanehara , W Xie and D. T.W. Ng
 

Additional factors combine with the core Hrd1 complex in a modular fashion, enabling it to recognize a variety of substrates.

 
 
 
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