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首页> 外文期刊>Molecular and Cellular Biology >Scd1 Plays a Tumor-Suppressive Role in Survival of Leukemia Stem Cells and the Development of Chronic Myeloid Leukemia
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Scd1 Plays a Tumor-Suppressive Role in Survival of Leukemia Stem Cells and the Development of Chronic Myeloid Leukemia

机译：Scd1在白血病干细胞的生存和慢性粒细胞白血病的发展中发挥肿瘤抑制作用。

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Chronic myeloid leukemia (CML) is derived from a stem cell, and it is widely accepted that the existence of leukemia stem cells (LSCs) is one of the major reasons for the relapse of CML treated with kinase inhibitors. Key to eradicating LSCs is to identify genes that play a critical role in survival regulation of these stem cells. Using BCR-ABL-induced CML mouse model, here we show that expression of the stearoyl-CoA desaturase 1 (Scd1) gene is downregulated in LSCs and that Scd1 plays a tumor-suppressive role in LSCs with no effect on the function of normal hematopoietic stem cells. Deletion of Scd1 causes acceleration of CML development and conversely overexpression of Scd1 delays CML development. In addition, using genetic approaches, we show that Pten, p53, and Bcl2 are regulated by Scd1 in LSCs. Furthermore, we find that induction of Scd1 expression by a PPARγ agonist suppresses LSCs and delays CML development. Our results demonstrate a critical role for Scd1 in functional regulation of LSCs, providing a new anti-LSC strategy through enhancing Scd1 activity.
机译：慢性粒细胞白血病（CML）来源于干细胞，并且广泛接受的是，白血病干细胞（LSCs）的存在是用激酶抑制剂治疗的CML复发的主要原因之一。根除LSC的关键是鉴定在这些干细胞的存活调节中起关键作用的基因。使用BCR-ABL诱导的CML小鼠模型，在这里我们显示硬脂酰辅酶A去饱和酶1（ Scd1 ）基因的表达在LSC中被下调，而Scd1在LSC中不具有肿瘤抑制作用。对正常造血干细胞功能的影响Scd1的删除会导致CML开发加速，反之，Scd1的过表达会延迟CML开发。此外，使用遗传方法，我们显示LSCs中的Scd1调控Pten，p53和Bcl2。此外，我们发现，PPARγ激动剂诱导Scd1表达可抑制LSC，并延迟CML的发展。我们的结果证明了Scd1在LSC功能调节中的关键作用，通过增强Scd1活性提供了一种新的抗LSC策略。

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