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Zhu Y.,Tianjin Huan Hu Hospital | Zhu Y.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | Yang P.,Tianjin Huan Hu Hospital | Yang P.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | And 17 more authors.
Anatomical Record | Year: 2013

The epithelial-mesenchymal transition (EMT) of tumor cells is deemed to be closely associated with tumor metastasis. CXCR4 has been proved to play an important role in the process of tumor metastasis. This study illustrates the function and expression of CXCR4 silencing and the EMT related genes in the human glioma cell line U87. The results showed that CXCR4 silencing could inhibit the cell invasive and adhesion potentials, expression of N-cadherin, vimentin, β-catenin, TGF-β1, p-Smad2, and p-Akt, and the activity of transcription factors NF-κB, AP-1, Snail, and twist. Meanwhile, CXCR4 silencing could also up-regulate the expression of E-cadherin, indicating that silencing of CXCR4 expression can inhibit the expression of EMT related genes in U87 cells. The study would provide a potential theoretical basis for the further exploration of the role of CXCR4 in human glioma. © 2013 Wiley Periodicals, Inc.


Zhu Y.,Tianjin Huan Hu Hospital | Zhu Y.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | Yang P.,Tianjin Huan Hu Hospital | Yang P.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | And 18 more authors.
Anatomical Record | Year: 2013

Tumor metastasis is the major cause of treatment failure and poor prognosis of glioma. Inhibiting metastasis has become an important therapeutic strategy for glioma treatment. CXCR4 has been proved to play an important role in the occurrence and development of tumors. In order to illustrate the effect of CXCR4 on glioma metastasis, we investigated the role of CXCR4 in U87 cells metastasis based on the CXCR4 silencing tumor cells. In this study, we found that CXCR4 silencing could suppress U87 cells invasion and adhesion potential, production of TGF-β1, IL-6, and IL-8, and blocked the G0/G1 phase of the cell cycle. We also found that CXCR4 silencing could up-regulate the mRNA and protein expression of p53, p21, and E-cadherin, and down-regulate the mRNA and protein expression of CD44 and MMP-2/-9. Meanwhile, CXCR4 silencing could decrease the phosphorylation of p-AKT and transcription activity of NF-κB promoter, and increased the phosphorylation of PTEN. The results provided a new research basis for the further study of CXCR4 gene, the screening of human glioma, as well as the target treatment for glioma and its prognosis. © 2013 Wiley Periodicals, Inc.


Wang Y.,University of Sichuan | Wang Y.,Tianjin Medical University | Zhu Y.,Tianjin Huanhu Hospital | Zhu Y.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | And 2 more authors.
International Journal of Clinical and Experimental Pathology | Year: 2015

Tongue squamous cell carcinoma is one of the most common cancers, which has the highest incidence in oral maxillofacial malignant tumors. MiR-21 may promote tumorigeness by down-regulating tumor suppressing genes and/or controlling the genes for cell differentiation and apoptosis, and it has been identified as the most expressive and unusual in a number of profiling experiments. The study shows there are high expressions of miR-21 in tongue squamous cell carcinoma cell lines (Tca8113 and its high metastatic lines), especially in high metastatic lines. miR-21 silencing could suppress the capacity of proliferation, migration and invasion, arrest the cell cycle and induce apoptosis of tongue squamous cell carcinoma cell lines (Tca8113 and its high metastatic lines). All the results indicate that miR-21 will probably open a new path to the gene therapy for oral squamous cell carcinoma.


Wang Q.,Tianjin Huanhu Hospital | Wang Q.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | Li X.,Tianjin Huanhu Hospital | Li X.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | And 4 more authors.
Molecular Medicine Reports | Year: 2014

Glioma is one of the most prevalent types of brain tumor and is associated with the highest mortality rate of all CNS cancers. Epithelial-mesenchymal transition (EMT) has been recognized as an important factor in tumor metastasis. Previously, it has been demonstrated that microRNA-16 (miR-16) has an important role in tumor metastasis in human cancer cell lines. However, the role of miR-16 in epithelial-mesenchymal transition of human glioma cells remains unclear. In the present study, U87 and U251 glioma cell lines overexpressing miR-16 were established and it was identified that miR-16 suppressed invasion, adhesion, cell cycle, production of interleukin (IL)-6, IL-8 and transforming growth factor-β, and EMT-related gene expression, including vimentin, β-catenin and E-cadherin in miR-16 overexpressing U87 and U251 glioma cells. Furthermore, miR-16 suppressed EMT mainly through the downregulation of p-FAK and p-Akt expression, and nuclear factor-κB and Slug transcriptional activity. Therefore, miR-16 may be an important therapeutic target and predictor for glioma therapy.

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