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논문 기본 정보

자료유형
학술저널
저자정보
Mingqi Qu (Henan Provincial People's Hospital) Ju Yu (Second Affiliated Hospital of Soochow University) Hongyuan Liu (Mianyang Central Hospital) Ying Ren (People's Hospital of Zhengzhou University) Chunxiao Ma (Henan Provincial People's Hospital) Xingyao Bu (Henan Provincial People's Hospital) Qing Lan (Second Affiliated Hospital of Soochow University)
저널정보
한국분자세포생물학회 Molecules and Cells Molecules and Cells 제40권 제10호
발행연도
2017.10
수록면
761 - 772 (12page)
DOI
10.14348/molcells.2017.0104

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Glioblastoma is the most frequent and most ag-gressive brain tumor in adults. Solute carrier family 8 member 2 (SLC8A2) is only expressed in normal brain, but not present in other human normal tissues or in gliomas. Therefore, we hy-pothesized that SLC8A2 might be a glioma tumor suppressor gene and detected the role of SLC8A2 in glioblastoma and explored the underlying molecular mechanism. The glioblas-toma U87MG cells stably transfected with the lentivirus plasmid containg SLC8A2 (U87MG-SLC8A2) and negative control (U87MG-NC) were constructed. In the present study, we found that the tumorigenicity of U87MG in nude mice was totally inhibited by SLC8A2. Overexpression of SLC8A2 had no effect on cell proliferation or cell cycle, but impaired the invasion and migration of U87MG cells, most likely through inactivating the extracellular signal-related kinases (ERK)1/2 signaling pathway, inhibiting the nuclear translocation and DNA binding activity of nuclear factor kappa B (NF-κB), reducing the level of matrix metalloproteinases (MMPs) and urokinase-type plasminogen activator (uPA)-its receptor (uPAR) system (ERK1/2-NF-κB-MMPs/uPA-uPAR), and altering the protein levels of epithelial to mesenchymal transitions (EMT)-associated proteins E-cardherin, vimentin and Snail. In addition, SLC8A2 inhibited the angiogenesis of U87MG cells, probably through combined inhibition of endothelium-dependent and endothelium-nondependent angiogenesis (vascular mimicry pattern). Totally, SLC8A2 serves as a tumor suppressor gene and inhibits invasion, angiogenesis and growth of glioblastoma.

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