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The role of CSE1L silencing in the regulation of proliferation and apoptosis via the AMPK/mTOR signaling pathway in chronic myeloid leukemia.
Hematology Pub Date : 2023-12-01 , DOI: 10.1080/16078454.2022.2161201
Xiao-Yu Liu 1 , Yong-Hong Wang 2 , Jing Wang 3 , Ji-Kun Quan 3 , Xu-Dong Li 3 , Kun-Ping Guan 2
Affiliation  

OBJECTIVES 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. MATERIALS AND METHODS 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. RESULTS 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. CONCLUSIONS 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.

中文翻译:

CSE1L 沉默在慢性粒细胞白血病中通过 AMPK/mTOR 信号通路调节增殖和凋亡的作用。

目的 染色体分离 1 样 (CSE1L) 在实体瘤中含量丰富且表达强烈。然而,CSE1L 在慢性粒细胞白血病 (CML) 中的表达和作用仍知之甚少。材料和方法 通过流式细胞术测量原发性 CML 患者和非血液学对照患者骨髓粒细胞中 CSE1L 的相对表达水平。应用细胞计数 kit-8 分析、DNA 含量定量测定和膜联蛋白 V-PE/7-AAD 染色来评估 CSE1L 敲低对细胞增殖、细胞周期进程和细胞凋亡的影响。结果原发性CML患者骨髓粒细胞CSE1L表达升高。在 CML 细胞系 K562 细胞中,CSE1L 敲低受损的细胞增殖阻断了细胞周期从 G0/G1 期向 S 期的转变,并促进细胞凋亡。CSE1L 的组合式降低 Bcl-2 蛋白表达并增加 Bax 蛋白表达。同时,CSE1L的敲低增强了磷酸化AMPK蛋白的表达并降低了磷酸化mTOR蛋白的表达。总 AMPK 和 mTOR 蛋白的表达不受影响。此外,伊马替尼处理的 K562 细胞中 CSE1L 表达水平降低。结论 CSE1L 在 K562 细胞存活和生长中起关键作用。这些功能可能部分依赖于AMPK/mTOR信号通路来实现。此外,CSE1L 可能对 CML 患者的治疗产生未来影响。CSE1L的敲低增强了磷酸化AMPK蛋白的表达并降低了磷酸化mTOR蛋白的表达。总 AMPK 和 mTOR 蛋白的表达不受影响。此外,伊马替尼处理的 K562 细胞中 CSE1L 表达水平降低。结论 CSE1L 在 K562 细胞存活和生长中起关键作用。这些功能可能部分依赖于AMPK/mTOR信号通路来实现。此外,CSE1L 可能对 CML 患者的治疗产生未来影响。CSE1L的敲低增强了磷酸化AMPK蛋白的表达并降低了磷酸化mTOR蛋白的表达。总 AMPK 和 mTOR 蛋白的表达不受影响。此外,伊马替尼处理的 K562 细胞中 CSE1L 表达水平降低。结论 CSE1L 在 K562 细胞存活和生长中起关键作用。这些功能可能部分依赖于AMPK/mTOR信号通路来实现。此外,CSE1L 可能对 CML 患者的治疗产生未来影响。
更新日期:2023-01-19
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