首页> 外文期刊>The Journal of Clinical Investigation: The Official Journal of the American Society for Clinical Investigation >All in for nuclear PFKP-induced CXCR4 metastasis: a T cell acute lymphoblastic leukemia prognostic marker
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All in for nuclear PFKP-induced CXCR4 metastasis: a T cell acute lymphoblastic leukemia prognostic marker

机译:全包核 PFKP 诱导的 CXCR4 转移:一种 T 细胞急性淋巴细胞白血病预后标志物

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摘要

Phosphofructokinase 1 (PFK1) is expressed in T cell acute lymphoblastic leukemia (T-ALL), where its upregulation is linked with cancer progression. While PFK1 functions in the glycolysis pathway within the cytoplasm, it is also present in the nucleus where it regulates gene transcription. In this issue of the JCI, Xueliang Gao, Shenghui Qin, et al. focus their mechanism-based investigation on the nucleocytoplasmic shuttling aspect of the PFK1 platelet isoform, PFKP. Functional nuclear export and localization sequences stimulated CXC chemokine receptor type 4 (CXCR4) expression to promote T-ALL invasion that involved cyclin D3/CDK6, c-Myc, and importin-9. Since the presence of nuclear PFKP is associated with poor survival in T-ALL, nuclear PFKP-induced CXCR4 expression might serve as a prognostic marker for T-ALL. More promising, though, are the mechanistic insights suggesting that approaches to dampening metastatic migration may have application to benefit patients with T-ALL.
机译:磷酸果糖激酶 1 (PFK1) 在 T 细胞急性淋巴细胞白血病 (T-ALL) 中表达,其上调与癌症进展有关。虽然 PFK1 在细胞质内的糖酵解途径中发挥作用,但它也存在于细胞核中,在那里它调节基因转录。在本期 JCI 中,Xueliang Gao、Shenghui Qin 等人将他们基于机制的研究重点放在 PFK1 血小板亚型 PFKP 的核质穿梭方面。功能性核输出和定位序列刺激 CXC 趋化因子受体 4 型 (CXCR4) 表达,促进涉及细胞周期蛋白 D3/CDK6、c-Myc 和 importin-9 的 T-ALL 侵袭。由于核 PFKP 的存在与 T-ALL 的生存率低相关,因此核 PFKP 诱导的 CXCR4 表达可能作为 T-ALL 的预后标志物。然而,更有希望的是,机制上的见解表明,抑制转移性迁移的方法可能适用于使T-ALL患者受益。

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