Department of Hematology, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Department of Gynecology, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi, China.
Braz J Med Biol Res. 2020 Jun 26;53(8):e9299. doi: 10.1590/1414-431X20209299. eCollection 2020.
The aim of this study was to evaluate the pathogenic role of newly identified long non-coding (lnc)-RNA LINCO1268 in acute myeloid leukemia (AML), and investigate its therapeutic potential. The expression level of LINC01268 in AML was measured by quantitative PCR (qPCR). The viability, cell cycle progression, and apoptosis of AML cells were measured by CCK-8 assay and flow cytometry, respectively. The interaction between LINC01268 and miR-217 were predicted by the miRDB website, and then verified by luciferase reporter assay and RNA immunoprecipitation (RIP) assay. The relationship between miR-217 and SOS1 was predicted by TargetScan website, and verified by luciferase reporter assay. LINC01268 was significantly upregulated by 1.6 fold in bone marrow samples of AML patients, which was associated with poor prognosis. LINC01268 was also significantly upregulated in AML cells. LINC01268 knockdown inhibited viability and cell cycle progression but promoted apoptosis of AML cells. Furthermore, LINC01268 functioned as a ceRNA via competitively binding to miR-217, and SOS1 was identified as a target of miR-217. Moreover, LINC01268 positively regulated SOS1 expression to promote AML cell viability and cell cycle progression but inhibited apoptosis via sponging miR-217. LINC01268 promoted cell growth and inhibited cell apoptosis through modulating miR-217/SOS1 axis in AML. This study offers a novel molecular mechanism for a better understanding of the pathology of AML. LINC01268 could be considered as a potential biomarker for the therapy and diagnosis of AML.
本研究旨在评估新鉴定的长链非编码（lnc）RNA LINCO1268 在急性髓系白血病（AML）中的致病作用，并探讨其治疗潜力。通过实时定量 PCR（qPCR）测定 AML 中 LINC01268 的表达水平。通过 CCK-8 测定和流式细胞术分别测定 AML 细胞的活力、细胞周期进程和凋亡。miRDB 网站预测 LINC01268 与 miR-217 的相互作用，然后通过荧光素酶报告基因测定和 RNA 免疫沉淀（RIP）测定验证。TargetScan 网站预测 miR-217 与 SOS1 的关系，并通过荧光素酶报告基因测定验证。在 AML 患者的骨髓样本中，LINC01268 显著上调 1.6 倍，与预后不良相关。LINC01268 在 AML 细胞中也显著上调。LINC01268 敲低抑制 AML 细胞活力和细胞周期进程，但促进凋亡。此外，LINC01268 通过竞争性结合 miR-217 作为 ceRNA 发挥作用，SOS1 被鉴定为 miR-217 的靶标。此外，LINC01268 通过海绵 miR-217 正向调节 SOS1 表达，促进 AML 细胞活力和细胞周期进程，但抑制凋亡。LINC01268 通过调节 miR-217/SOS1 轴促进 AML 细胞生长并抑制细胞凋亡。本研究为更好地理解 AML 的病理学提供了新的分子机制。LINC01268 可作为 AML 治疗和诊断的潜在生物标志物。
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