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- 저자 : Xian-Biao Shi (검색결과 2 건)
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MicroRNA-206 Reduces Osteosarcoma Cell Malignancy In Vitro by Targeting the PAX3-MET Axis
Qian-Rong Deng,Fang-Biao Zhan,Xian-Wei Zhang,Shi-Long Feng,Jun Cheng,You Zhang,Bo Li,Li-Zhong Xie 연세대학교의과대학 2019 Yonsei medical journal Vol.60 No.2
Purpose: This study was undertaken to explore how miR-206 represses osteosarcoma (OS) development. Materials and Methods: Expression levels of miR-206, PAX3, and MET mRNA were explored in paired OS and adjacent tissuespecimens. A patient-derived OS cell line was established. miR-206 overexpression and knockdown were achieved by lentiviraltransduction. PAX3 and MET overexpression were achieved by plasmid transfection. Treatment with hepatocyte growth factor(HGF) was utilized to activate c-Met receptor. Associations between miR-206 and PAX3 or MET mRNA in OS cells were verifiedby AGO2-RNA immunoprecipitation assay and miRNA pulldown assay. OS cell malignancy was evaluated in vitro by cell proliferation,metastasis, and apoptosis assays. PAX3 and MET gene expression in OS cells was assayed by RT-qPCR and Western blot. Activation of PI3K-AKT and MAPK-ERK in OS cells were assayed by evaluating Akt1 Ser473 phosphorylation and total threoninephosphorylation of Erk1/2, respectively. Results: Expression levels of miR-206 were significantly decreased in OS tissue specimens, compared to adjacent counterparts,and were inversely correlated with expression of PAX3 and MET mRNA. miR-206 directly interacted with PAX3 and MET mRNAin OS cells. miR-206 overexpression significantly reduced PAX3 and MET gene expression in OS cells in vitro, resulting in significantdecreases in Akt1 and Erk1/2 activation, cell proliferation, and metastasis, as well as increases in cell apoptosis, while miR-206 knockdown showed the opposite effects. The effects of miR-206 overexpression on OS cells were reversed by PAX3 or METoverexpression, but only partially attenuated by HGF treatment. Conclusion: miR-206 reduces OS cell malignancy in vitro by targeting PAX3 and MET gene expression.
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Dynamic analysis for gene expression profiles of endothelial colony forming cells under hypoxia
De-Cai Yu,Wen-Du Feng,Xian-Biao Shi,hi-Yong Wang,Wei Ge,Chun-Ping Jiang,Xi-Tai Sun,Yi-Tao Ding 한국유전학회 2013 Genes & Genomics Vol.35 No.4
Previous studies have shown that endothelial colony forming cells (ECFCs) play an important role in the neovascularization of tumors. Hypoxia is emphasized as an important promoter of angiogenesis. However, little is known about genome-wide transcriptional regulation of ECFCs under hypoxic conditions. In this study, gene expression profiles in ECFCswere evaluated under hypoxic conditions for 3, 6, 12, 24,and 48 h, using Affymetrix U133 plus 2.0 chip microarray. 1,103 hypoxia-regulated genes were filtered, with 379(0.693 %) genes up-regulated and 724 (1.32 %) genes downregulated. Most of the up-regulated genes were involved in apoptosis, cell proliferation, or metabolic processes, while most of the down-regulated genes were involved in cell adherence,cell cycle,DNAandmRNAmetabolic processes,multi-cellular organism development, protein metabolic processes, response to stress, signal transduction, or transport. This expression profile is ECFC-specific, because it is significantly different from those of endothelial cells and smooth muscle cells under hypoxic conditions. Moreover, hypoxia-regulated apoptosis in ECFCs is mainly related with the mitochondrial pathway (p53-BAX-Caspase-9) and the death receptor pathway (FASCaspase-8-Caspase-3). MAPK pathway is activated in ECFCs under hypoxic conditions. The differentially expressed genes of ECFCs were identified under hypoxic conditions, and related with cell apoptosis, cell cycle and MAPK pathways, shedding light on the mechanism of angiogenesis.
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