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首页> 外文期刊>Leukemia Research: A Forum for Studies on Leukemia and Normal Hemopoiesis >Sam68 affects cell proliferation and apoptosis of human adult T-acute lymphoblastic leukemia cells via AKT/mTOR signal pathway
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Sam68 affects cell proliferation and apoptosis of human adult T-acute lymphoblastic leukemia cells via AKT/mTOR signal pathway

机译:Sam68通过AKT / mTOR信号通路影响成人T急性淋巴细胞白血病细胞的增殖和凋亡

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摘要

Sam68 (Src associated in mitosis, 68 kDa) belongs to the signal, transduction and activation of RNA (STAR) family and its function has been linked to the onset and progression of many tumors. However, the role of Sam68 in T-acute lymphoblastic leukemia (T-ALL) remains unclear. This present study aimed to investigate whether and how Sam68 involved in T-ALL. Our results showed high expression of Sam68 in adult T-ALL cases, Jurkat and CCRF-CEM cell lines. Knockdown of Sam68 repressed cell proliferation, increased apoptosis, induced S arrest along with upregulation of p21, Bad, cleaved caspase-9, caspase-3, PARP and downregulation of CDK2 and Bcl-xl. Furthermore, the data indicated that the expression change of Sam68 went with the changes of AKT/mTOR signaling pathway in T-ALL cell lines. Our findings demonstrated that Sam68 possibly participated in the progresses of T-ALL at least partially via AKT/mTOR signaling pathway. (C) 2016 Elsevier Ltd. All rights reserved.
机译:Sam68(与有丝分裂相关的Src,68 kDa)属于RNA(STAR)家族的信号,转导和激活,其功能与许多肿瘤的发生和发展有关。但是,尚不清楚Sam68在T型急性淋巴细胞白血病(T-ALL)中的作用。本研究旨在调查Sam68是否以及如何参与T-ALL。我们的结果显示,Sam68在成年T-ALL,Jurkat和CCRF-CEM细胞系中高表达。敲除Sam68可抑制细胞增殖,增加细胞凋亡,诱导S阻滞,同时上调p21,Bad,裂解的caspase-9,caspase-3,PARP以及CDK2和Bcl-xl的下调。此外,数据表明在T-ALL细胞系中,Sam68的表达变化与AKT / mTOR信号传导途径的变化一致。我们的发现表明,Sam68可能至少部分通过AKT / mTOR信号通路参与了T-ALL的进展。 (C)2016 Elsevier Ltd.保留所有权利。

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