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Publications (3)3.59 Total impact

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    ABSTRACT: Osteosarcoma (OS) is the most common primary malignant bone tumor that has poor prognosis. Molecular mechanisms underlying disease progression remain largely unknown. Sox9, one of the Sox family transcription factors, is closely associated with the development of a variety of malignant tumors. This study investigates the expression of Sox9, Wnt1 and Fzd1 in human osteosarcoma tissues and cells and the role of Sox9 in the proliferation of human osteosarcoma cells. Immunohistochemical analyses for Sox9, Wnt1, Fzd1, and Ki-67 proteins were performed in human primary osteosarcoma tissues from 48 patients. The small interfering RNA (siRNA) of Sox9 was transfected into human osteosarcoma MG63 cells. At 24 and 48 h after transfection with Sox9 siRNA, the expression of Wnt1 and Fzd1 was analyzed by RT-qPCR, Western blot, and immunofluorescence techniques. Cell proliferation was assayed by CCK-8 method, and Ki-67 protein expression was analyzed by Western blot. Results showed that the expressions of Sox9, Wnt1, Fzd1, and Ki-67 proteins in human osteosarcoma tissues were higher than those in the adjacent non-cancerous tissues. Hyperexpressions of Sox9, Wnt1, Fzd1, and Ki-67 proteins occurred more frequently in human osteosarcoma tissues with an advanced clinical stage (IIb/III). Sox9 siRNA reduced both mRNA and protein expression levels of Wnt1 and Fzd1, which result in the distinct inhibition of MG63 cell proliferation. Our study suggests that Sox9 siRNA inhibits the proliferation capability of human osteosarcoma cells by down-regulating the expression of Wnt1 and its receptor Fzd1, which may provide new gene targets for the clinical treatment of osteosarcoma.
    International journal of clinical and experimental pathology. 01/2014; 7(8):4795-805.
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    ABSTRACT: Our aim was to examine the change in expression of molecules involved in Wnt signaling in the pathogenesis of amyotrophic lateral sclerosis (ALS) in adult transgenic mice, and to reveal the relationship between the Wnt signaling pathway and the pathogenesis of ALS. We determined the expression of Wnt2, Wnt7a, and GSK-3beta in the spinal cord of SOD1(G93A) ALS transgenic mice at different ages using reverse transcriptase-polymerase chain reaction, western blot, and immunohistochemistry. Using double labeling, we determined whether Wnt2, Wnt7a, and GSK-3beta were colocalized with beta-tubulin III, for neurons, or glial fibrillary acidic protein, for mature astrocytes. Wnt2, Wnt7a mRNA and protein in the spinal cord of ALS mice were upregulated and compared with wild-type mice. Phospho-GSK-3beta (Ser 9) protein levels in the spinal cord of ALS mice were upregulated. Moreover, the immunoreactivity of Wnt2, Wnt7a, and phospho-GSK-3beta (Ser 9) was strong in ALS mice but weak in wild-type mice at the same time points. Double immunofluorescence labeling showed that Wnt2 and Wnt7a were expressed in both neurons and astrocytes, whereas GSK-3beta was expressed only in neurons. Most of the double positive cells were located in the ventral horns of the gray matter, the locus of neurodegeneration. Neurodegeneration upregulated the expression of Wnt2 and Wnt7a in the spinal cord of ALS mice, which in turn activated Wnt signaling, and accordingly inhibited GSK-3beta activity in disease progression of ALS in adult transgenic mice; this could regulate the downstream gene of the Wnt signaling pathway and promote cell proliferation.
    Neurological Research 05/2012; 34(4):390-9. · 1.18 Impact Factor
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    ABSTRACT: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the progressive and fatal loss of motor neurons. In ALS, there is a significant cell proliferation in response to neurodegeneration; however, the exact molecular mechanisms of cell proliferation and differentiation are unclear. The Wnt signaling pathway has been shown to be involved in neurodegenerative processes. Wnt3a, β-catenin, and Cyclin D1 are three key signaling molecules of the Wnt/β-catenin signaling pathway. We determined the expression of Wnt3a, β-catenin, and Cyclin D1 in the adult spinal cord of SOD1(G93A) ALS transgenic mice at different stages by RT-PCR, Western blot, and immunofluorescence labeling techniques. We found that the mRNA and protein of Wnt3a and Cyclin D1 in the spinal cord of the ALS mice were upregulated compared to those in wild-type mice. In addition, β-catenin translocated from the cell membrane to the nucleus and subsequently activated transcription of the target gene, Cyclin D1. BrdU and Cyclin D1 double-positive cells were increased in the spinal cord of these mice. Moreover, Wnt3a, β-catenin, and Cyclin D1 were also expressed in both neurons and astrocytes. The expression of Wnt3a, β-catenin or Cyclin D1 in mature GFAP(+) astrocytes increased. Moreover, BrdU/Cyclin D1/GFAP triple-positive cells were detected in the ALS mice. Our findings suggest that neurodegeneration activates the Wnt/β-catenin signaling pathway, which is associated with glial proliferation in the adult spinal cord of ALS transgenic mice. This mechanism may be significant in clinical gene therapy.
    Biochemical and Biophysical Research Communications 03/2012; 420(2):397-403. · 2.41 Impact Factor