基因敲除
PI3K/AKT/mTOR通路
安普克
细胞凋亡
髓样
细胞生长
髓系白血病
癌症研究
造血
K562细胞
医学
流式细胞术
白血病
细胞生物学
信号转导
生物
蛋白激酶A
免疫学
激酶
干细胞
生物化学
作者
Xiaoyu Liu,Yonghong Wang,Jing Wang,Ji-Kun Quan,Xudong Li,Kun-Ping Guan
出处
期刊:Hematology
[Informa]
日期:2023-01-18
卷期号:28 (1): 1-9
被引量:1
标识
DOI:10.1080/16078454.2022.2161201
摘要
Chromosome segregation 1-like (CSE1L) is abundant and strongly expressed in solid tumors. However, the expression and role of CSE1L in chronic myeloid leukemia(CML) remain largely unknown.The relative expression levels of CSE1L in bone marrow granulocytes from patients with primary CML and non-hematologic controls were measured by flow cytometry. Cell counting kit-8 analysis, DNA Content Quantitation Assay, and Annexin V-PE/7-AAD staining were applied to assess the effects of CSE1L knockdown on cell proliferation, cell cycle progression, and apoptosis.Elevated expression of CSE1L was detected in bone marrow granulocytes of patients with primary CML. In the CML cell line K562 cells, CSE1L knockdown impaired cell proliferation blocked the cell cycle shift from G0/G1 phase to the S phase, and promoted apoptosis. Knockdown of CSE1L reduced Bcl-2 protein expression and increased Bax protein expression. Meanwhile, knockdown of CSE1L enhanced the expression of phospho-AMPK protein and decreased the expression of phospho-mTOR protein. The expression of total AMPK and mTOR proteins was not affected. In addition, CSE1L expression levels were decreased in imatinib-treated K562 cells.CSE1L plays a pivotal role in K562 cell survival and growth. These functions may be partially dependent on the AMPK/mTOR signaling pathway to achieve. In addition, CSE1L may have had a future impact on the treatment of CML patients.
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