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Wang Y.,University of Sichuan | Wang Y.,Tianjin Medical University | Zhu Y.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | Lv P.,Tianjin Medical University | Li L.,University of Sichuan
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. Source


Liu A.,Tianjin Medical University | Zhang X.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | Qi L.,Tianjin Medical University | Liu Y.,Taishan Medical University
Tumor Biology | Year: 2015

Benzyl isothiocyanate (BITC) has been shown to have inhibitory potential for human glioma U87MG cells; however, the effect and mechanism were not fully clear. In the present study, we found that BITC could inhibit U87MG cell proliferation, adhesion, invasion, and vasculogenic mimicry (VM) formation potential and induce oxidative stress, apoptosis, and cell cycle arrest. We also found that the expression of proliferation, invasion, VM oxidative stress, apoptosis, and cell cycle-related gene and the activity of tumor-related signaling pathways, including protein kinase C (PKC) ζ and Akt/nuclear factor-kappa B (NF-κB) pathways, were suppressed by BITC treatment. We also explored the anti-tumor potential of BITC in vivo, and we found that BITC also could regulate the expression of tumor-related gene and angiogenesis in nude mice model. Finally, we optimized the BITC construction targeting alkylglycerone phosphate synthase (AGPS) by computer-aided design, and the derivants also showed anti-tumor potential in vitro. © 2014, International Society of Oncology and BioMarkers (ISOBM). Source


Zhang X.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | Qi L.,Tianjin Medical University | Cai Y.,Tianjin Neurosurgery Institute | Xuan G.,Tianjin Medical University | Jiang Y.,Tianjin Medical University
Oncotarget | Year: 2016

Tumor angiogenesis plays a critical role in the tumor progression. Highly upregulated in liver cancer (HULC) is a long noncoding RNA (lncRNA) that acts as an oncogene in gliomas. We found that HULC, vascular endothelial growth factor (VEGF), and ESM-1 (endothelial cell specific molecule 1) expression and microvessel density were positively correlated with grade dependency in glioma patient tissues, and that HULC silencing suppressed angiogenesis by inhibiting glioma cells proliferation and invasion. This process induced anoikis and blocked the cell cycle at G1/S phase via the PI3K/Akt/mTOR signaling pathway, thus regulating the tumor-related genes involved in the above biological behavior in human glioma U87MG and U251 cells. However, these effects were reversed by ESM-1 overexpression, suggesting a mediating role of ESM-1 in the pro-angiogenesis effect of HULC. Our results define the mechanism of the pro-angiogenesis activity of HULC, which shows potential for application as a therapeutic target in glioma. Source


Zhu Y.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | Yang P.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | Zhang X.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | Zhang L.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | And 8 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. Source


Zhu Y.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | Yang P.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | Wang Q.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | Hu J.,Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration | And 8 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. Source

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