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RISS 인기검색어
- 검색키워드
- 저자 : Ge Zhi-Qiang (검색결과 3 건)
- 무료
- 기관 내 무료
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AntagomiR-27a Targets FOXO3a in Glioblastoma and Suppresses U87 Cell Growth in Vitro and in Vivo
Ge, Yun-Fei,Sun, Jun,Jin, Chun-Jie,Cao, Bo-Qiang,Jiang, Zhi-Feng,Shao, Jun-Fei Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.2
Objective: To study the effect of the antagomiR-27a inhibitor on glioblastoma cells. Methods: The miR-27a expression level in specimens of human glioblastoma and normal human brain tissues excised during decompression for traumatic brain injury was assessed using qRT-PCR; The predicted target gene of miR-27a was screened out through bioinformatics databases, and the predicted gene was verified using genetic report assays; the effect of antagomiR-27a on the invasion and proliferation of glioma cells was analyzed using MTT assays and 5-ethynyl-2'-deoxyuridine (EdU) labeling. A xenograft glioblastoma model in BALB-c nude mice was established to detect the effect of antagomiR-27a on tumour growth. Results: qRT-PCR results showed that miR-27a significantly increased in specimens from glioblastoma comparing with normal human brain tissues. Th miR-27a inhibitor significantly suppressed invasion and proliferation of glioblastoma cells. FOXO3a was verified as a new target of miR-27a by Western blotting and reporter analyzes. Tumor growth in vivo was suppressed by administration of the miR-27a inhibitor. Conclusion: MiR-27a may be up-regulated in human glioblastoma, and antagomiR-27a could inhibit the proliferation and invasion ability of glioblastoma cells.
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Li Jing-Chuan,Ge Zhi-Qiang,Yuan Ying-Jin The Korean Society for Biotechnology and Bioengine 2005 Biotechnology and Bioprocess Engineering Vol.10 No.2
Ion fluxes across the plasma membrane activated by 1 mM $Ce^{4+}$, cell apoptosis and taxol biosynthesis in suspension cultures of Taxus cusp/data were studied. The extracellular pH sharply decreased upon the addition of 1 mM $Ce^{4+}$, then increased gradually and exceeded the initial pH value over a time period of 12 h. The extracellular $Ca^{2+}$ concentration decreased within the first 3 h after the addition of $Ce^{4+}$, then gradually decreased to one third of initial value in control at about 72 h and remained unchanged afterwards. Experiments with an ion channel blocker and a $Ca^{2+}$-channel blocker indicated that the dynamic changes in extracellular pH and the $Ca^{2+}$ concentration resulted from the $Ce^{4+}$-induced activation of W uptake and $Ca^{2+}$ influx across the plasma membrane via ion channels. A pretreatment of the ion channel blocker initiated $Ce^{4+}$-treated cells to undergo necrosis, and the prior addition of the $Ca^{2+}$-channel blocker inhibited $Ce^{4+}$-induced taxol biosynthesis and apoptosis. It is thus inferred that W uptake is necessary for cells to survive a $Ce^{4+}$-caused acidic environment and is one of the mechanisms of $Ce^{4+}$-induced apoptosis. Furthermore, the $Ca^{2+}$ influx across the plasma membrane mediated both the $Ce^{4+}$-induced apoptosis and taxol biosynthesis.
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Ying-Jin Yuan,Jing-Chuan Li,Zhi-Qiang Ge 한국생물공학회 2005 Biotechnology and Bioprocess Engineering Vol.10 No.2
Ion fluxes across the plasma membrane activated by 1 mM Ce4+, cell apoptosis and taxol biosynthesis in suspension cultures of Taxus cuspidata were studied. The extracellular pH sharply decreased upon the addition of 1 mM Ce4+, then increased gradually and exceeded the initial pH value over a time period of 12 h. The extracellular Ca2+ concentration decreased within the first 3 h after the addition of Ce4+, then gradually decreased to one third of initial value in control at about 72 h and remained unchanged afterwards. Experiments with an ion channel blocker and a Ca2+-channel blocker indicated that the dynamic changes in extracellular pH and the Ca2+ concentration resulted from the Ce4+-induced activation of H+ uptake and Ca2+ influx across the plasma membrane via ion channels. A pretreatment of the ion channel blocker initiated Ce4+-treated cells to undergo necrosis, and the prior addition of the Ca2+-channel blocker inhibited Ce4+-induced taxol biosynthesis and apoptosis. It is thus inferred that H+ uptake is necessary for cells to survive a Ce4+-caused acidic environment and is one of the mechanisms of Ce4+-induced apoptosis. Furthermore, the Ca2+ influx across the plasma membrane mediated both the Ce4+-induced apoptosis and taxol biosynthesis.
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