Metallothionein 3 Is a Hypoxia-Upregulated Oncogene Enhancing Cell Invasion and Tumorigenesis in Human Bladder Carcinoma Cells.
作者： Ke-Hung Tsui , Chen-Pang Hou , Kang-Shuo Chang , Yu-Hsiang Lin , Tsui-Hsia Feng
DOI: 10.3390/IJMS20040980
关键词:
摘要: Metallothioneins have been viewed as modulators in a number of biological regulations regarding cancerous development; however, the function metallothionein 3 (MT3) bladder cancer is unexplored. We determined regulatory mechanisms and potential MT3 carcinoma cells. Real-Time Reverse Transcriptase-Polymerase Chain Reaction (RT-qPCR) assays revealed that TSGH-8301 cells expressed more levels than RT-4, HT1376, T24 Immunoblot RT-qPCR showed arsenic (AS2O3) treatments enhanced gene expression MT3. Hypoxia induced HIF-1α, HIF-2α, expression; furthermore, HIF-2α-knockdown attenuated hypoxic activation on expression. Ectopic overexpression increased cell proliferation, invasion, tumorigenesis significantly HT1376 vitro vivo; MT3-knockdown had reverse effect. Moreover, knockdown arsenic-induced apoptosis by Annexin V-FITC assay. MT3-overexpression downregulated expressions N-myc downstream regulated 1 (NDRG1), 2 (NDRG2), mammary serine protease inhibitor (MASPIN) cells, whereas opposite The experiments indicated an arsenic- hypoxia-upregulated oncogene promotes growth invasion via downregulation NDRG1, NDRG2, MASPIN expressions.
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