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Knockdown of Adhesion-Regulating Molecule 1 Inhibits Proliferation in HL60 Cells

机译:击倒的粘附调节分子1抑制HL60细胞的增殖。

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Background/Aims: Adhesion-regulating molecule 1 (ADRM1), a receptor located on the 26S proteasome, is upregulated in many solid cancers. However, little is known about its role in acute leukemia (AL). Methods: We determined ADRM1 expression levels in both untreated AL samples and leukemia cell lines using real-time polymerase chain reaction or Western blot analysis. Growth curves, colony formation assays, cell cycle and apoptosis analyses, cell migration and invasion assays and NF-kappa B p65 nuclear translocation assays via Western blotting were used to examine the biological behavior of HL60 cells and the underlying mechanism. Results: ADRM1 was upregulated in both untreated AL samples and leukemia cell lines. ADRM1 knockdown significantly suppressed HL60 cell proliferation (48.82 +/- 12.58%) and colony formation and caused cell cycle arrest in the G0/G1 phase. Furthermore, we confirmed that ADRM1 knockdown suppressed p65 nuclear translocation. Conclusion: Our study revealed that ADRM1 was overexpressed in AL, especially in CD34+ leukemia stem and progenitor cells. ADRM1 may play a role in AL via the proteasome-ubiquitin pathway by potentially sustaining the activation of NF-kappa B signaling. (C) 2015 S. Karger AG, Basel
机译:背景/目的:在许多实体癌中,粘附调节分子1(ADRM1)(位于26S蛋白酶体上的受体)被上调。但是,对其在急性白血病(AL)中的作用了解甚少。方法:我们通过实时聚合酶链反应或蛋白质印迹分析确定了未经处理的AL样本和白血病细胞系中ADRM1的表达水平。生长曲线,集落形成测定,细胞周期和凋亡分析,细胞迁移和侵袭测定以及通过Western印迹的NF-κBp65核易位测定被用于检查HL60细胞的生物学行为及其潜在机制。结果:未处理的AL样品和白血病细胞系中的ADRM1均被上调。 ADRM1敲低显着抑制HL60细胞增殖(48.82 +/- 12.58%)和集落形成,并导致细胞周期停滞在G0 / G1期。此外,我们证实了ADRM1敲低抑制了p65核易位。结论:我们的研究表明,ADRM1在AL中过表达,尤其是在CD34 +白血病干细胞和祖细胞中。通过潜在地维持NF-κB信号传导的激活,ADRM1可能通过蛋白酶体-泛素途径在AL中发挥作用。 (C)2015 S.Karger AG,巴塞尔

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