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1. The roles of mitoferrin-2 in the process of arsenic trioxide-induced cell damage in human gliomas | |||
WANG Ligang | |||
Clinical Medicine 08 May 2017 | |||
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Abstract:Background: Among glioma treatment strategies, arsenic trioxide (As2O3) has shown efficacy as a therapeutic agent against human gliomas. However, the exact antitumor mechanism of action of As2O3 is still unclear. Mitochondria are considered to be the major source of intracellular reactive oxygen species (ROS), which are known to be associated with As2O3-induced cell damage. Therefore, we investigated whether mitoferrin-2, a mitochondrial iron uptake transporter, participates in As2O3-induced cell killing in human gliomas. Methods: Human glioma cell lines were used to explore the mechanism of As2O3's antitumor effects. First, expression of mitoferrin-2 was analyzed in glioma cells that were pretreated with As2O3. Changes in ROS production and apoptosis were assessed. Furthermore, cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). Results: In the present study we found that As2O3 induced ROS production and apoptosis in glioma cells. In addition, gene expression of mitoferrin-2, a mitochondrial iron uptake transporter, was increased 4 to 5 fold after exposure to As2O3 (5 μM) for 48 hours. Furthermore, apoptosis and cytotoxicity induced by As2O3 in glioma cells were decreased after silencing the mitoferrin-2 gene. Conclusions: Our findings indicated that mitoferrin-2 participates in mitochondrial ROS-dependent mechanisms underlying As2O3-mediated damage in glioma cells. | |||
TO cite this article:WANG Ligang. The roles of mitoferrin-2 in the process of arsenic trioxide-induced cell damage in human gliomas[OL].[ 8 May 2017] http://en.paper.edu.cn/en_releasepaper/content/4733708 |
2. The role of miR-451 in the switch between proliferation and migration in malignant glioma cells depends essentially on AMPK signaling which thereby modulates mTOR and Rac1 activation | |||
Zhao Kai,Wang Leilei,Li Tao,Zhu Meng,Zhang Chen,Chen Lei,Zhao Pengfei,Zhou Hua,Yu Shengping,Yang Xuejun | |||
Clinical Medicine 10 January 2017 | |||
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Abstract:Glioblastoma multiforme (GBM), WHO grade IV astrocytoma, is the most common primary neoplasm of the central nervous system (CNS), which has the highest malignancy and mortality rates. It is the invasive nature of GBM still complicates surgical resection and restricts chemotherapeutic access contributing to gloomy outcomes. The migration of tumor cells is closely related to the tumors proliferation. The alteration of cell phenotype is proposed to be a crucial mechanism with some of intracellular factors during this invasive progession. Using qRT-PCR analysis, we found that the expression of miR-451 in glioma tissues was lower than control brain tissues, especially in central area. In glioma cell lines, we found that decreased miR-451 expression suppressed tumor cells proliferation but enhanced the migration with low level of mTOR activation and high level of Rac1 activation respectively. Interestingly, the effect of miR-451 on glioma cytological behaviors and activation of mTOR and Rac1 was narrowed when we knocked down the AMPKa1 expression with a synthetic shRNA. We suggest that the different micro niche of glioma result in the heterogeneity of miR-451 expression. Our data indicated that miR-451, through adjusting the activity of AMPK, the hub regulator in the downstream pathway, reconfigures the activation of mTOR and Rac1, which play key roles on proliferation and migration respectively in glioma cells adapting to environment condition in the tumor. Whether a therapeutic target would promote cell infiltration has to be considered when we focus on the suppression of tumor cells proliferation. | |||
TO cite this article:Zhao Kai,Wang Leilei,Li Tao, et al. The role of miR-451 in the switch between proliferation and migration in malignant glioma cells depends essentially on AMPK signaling which thereby modulates mTOR and Rac1 activation[OL].[10 January 2017] http://en.paper.edu.cn/en_releasepaper/content/4717205 |
3. Absorption of Subdural Hematoma in a Modified Rat Model | |||
Zhang Jianning,Wang Dong | |||
Clinical Medicine 30 March 2011 | |||
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Abstract:Studies on the pathophysiology of subdural hematoma (SDH) have primarily been focused on the acute phase, wherase the course of hematoma absorption remains poorly understood. In present study, we have modified a rat model of SDH to specifically investigate the correlation between neovascularization of hematom encapsulating membrane and cerebral tissue and hematoma absorption. The modified method significant improved the success rate from 10% to 71.4% and reduced surgical related injury. Depending on this more clinically relevant model of SDH, we demonstrated a non-linear reduction in reduction volume, with an initial slow rate in the first 6 days followed by rapid absorption. The neovascularization was characterized by the formation of arachnoid granulation-like structures at the interface between hematoma and encapsulating neomembrane. The recovery of sensorimotor deficits closely correlated with the neovascularization in the neomembranes, which dictates the rate of hematoma absorption. There was a close correlation between the increase in neovascularization and the absorption rate of SDH, suggesting that the development of neovasculature in the neomembrane plays a key role in hematoma absorption and measures to enhance the process could have therapeutic potentials. | |||
TO cite this article:Zhang Jianning,Wang Dong. Absorption of Subdural Hematoma in a Modified Rat Model[OL].[30 March 2011] http://en.paper.edu.cn/en_releasepaper/content/4419224 |
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