Assay of OAZ1 mRNA Levels in Chronic Myeloid Leukemia Combined with Application of Leukemia PCR Array Identified Relevant Gene Changes Affected by Antizyme

Assay of OAZ1 mRNA Levels in Chronic Myeloid Leukemia Combined with Application of Leukemia PCR Array Identified Relevant Gene Changes Affected by Antizyme
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DOI:
10.1159/000353406
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发表时间:
2013-10
期刊:
影响因子:
2.4
通讯作者:
Bingping Wu;Xing Wang;Wenli Ma;Wenling Zheng;Li Jiang
Bingping Wu;Xing Wang;Wenli Ma;Wenling Zheng;Li Jiang
中科院分区:
医学4区
文献类型:
--
作者:
Bingping Wu;Xing Wang;Wenli Ma;Wenling Zheng;Li Jiang

文献摘要

相似文献

鸟氨酸脱羧酶抗酶(OAZ)最近成为各种恶性肿瘤的潜在治疗靶点,因为它在细胞功能(包括增殖、分化、凋亡和基因组稳定性)中发挥着至关重要的作用。因此,人们对发现其在慢性粒细胞白血病(CML)中的功能非常感兴趣。首先,通过 qRT-PCR 在 43 例 CML 病例和 23 名对照者中检测 OAZ1 mRNA,我们证明 OAZ1 mRNA 在 CML 患者中显着下调。为了进一步了解其在 CML 发病机制中的功能,OAZ1 过表达,并且使用人白血病 PCR 阵列分析来监测通常参与白血病发展、分类和治疗反应的关键基因的表达。我们发现了几个有利的上调因子,包括 CXCL10、DAPK1 和 IKZF3。总之,OAZ1 可能是 CML 的一个有用的治疗靶点,因为它具有诱导红系分化和细胞凋亡的潜在能力。这些功能被证明与 OAZ1 直接或间接引起的几个基因变化有关。 OAZ1 如何影响其他基因的机制仍有待阐明。
Ornithine decarboxylase antizyme (OAZ) has recently emerged as a potential therapeutic target in various malignant tumors because it plays vital roles in cellular functions including proliferation, differentiation, apoptosis and genomic stability. Therefore, there is a significant interest in discovering its function in chronic myeloid leukemia (CML). Firstly, OAZ1 mRNA was measured by qRT-PCR in 43 cases with CML and 23 controls, and we demonstrated that it is significantly down-regulated in CML patients. To further understand its functions in CML pathogenesis, OAZ1 was overexpressed, and the human leukemia PCR array analysis was used to monitor the expression of key genes commonly involved in leukemia development, classification and therapeutic response. We found several favorable up-regulation factors including CXCL10, DAPK1 and IKZF3. In conclusion, OAZ1 may be a useful therapeutic target in CML due to its potential ability to induce erythroid differentiation and cell apoptosis. These functions were proven to be associated with several gene changes that were directly or indirectly caused by OAZ1. The mechanism of how OAZ1 affects other genes remains to be elucidated.