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Prognostic value of expression of nuclear factor kappa-B/p65 in non-GCB DLBCL patients.核因子κB/p65表达在非生发中心B细胞弥漫性大B细胞淋巴瘤患者中的预后价值
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Sphk1 promotes breast epithelial cell proliferation via NF-κB-p65-mediated cyclin D1 expression.鞘氨醇激酶1通过核因子κB-p65介导的细胞周期蛋白D1表达促进乳腺上皮细胞增殖。
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β-TrCP1 通过 TNF 依赖性 NF-κB 激活促进弥漫性大 B 细胞淋巴瘤细胞增殖。

β-TrCP1 promotes cell proliferation via TNF-dependent NF-κB activation in diffuse large B cell lymphoma.

机构信息

Department of Pathogenic Biology, Medical College, Nantong University, Nantong, Jiangsu, People's Republic of China.

Department of Pathology, Affiliated Tumor Hospital of Nantong University, Nantong, Jiangsu, People's Republic of China.

出版信息

Cancer Biol Ther. 2020;21(3):241-247. doi: 10.1080/15384047.2019.1683332. Epub 2019 Nov 15.

DOI:10.1080/15384047.2019.1683332
PMID:31731887
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7012105/
Abstract

Diffuse large B cell lymphoma (DLBCL), a heterogeneous group of invasive disease, is the most common type of B-cell non-Hodgkin's lymphomas. The mechanism of its development is closely related to the constitutive activation of NF-κB. In this study, we investigated the function and the mechanism of β-TRCP1 in DLBCL. CCK8 and EdU assays showed that β-TRCP1 could promote the growth of DLBCL cells under the stimulation of TNFα. Furthermore, overexpression of β-TRCP1 enhanced NF-κB activation in the presence of TNFα. Moreover, ectopic expression of β-TRCP1 decreased IκB-α expression but increased phospho-p65 expression. In addition, β-TRCP1 promoted cell cycle progression by accelerating G1-S phase transition. We also found that silencing of β-TrCP1 increased mitoxantrone-induced cell growth arrest and apoptosis. Based on these, we proposed that the expression of β-TRCP1 promoted cell proliferation via TNF-dependent NF-κB activation in DLBCL cells.

摘要

弥漫性大 B 细胞淋巴瘤（DLBCL）是一种异质性侵袭性疾病，是最常见的 B 细胞非霍奇金淋巴瘤类型。其发病机制与 NF-κB 的组成性激活密切相关。在本研究中，我们研究了β-TRCP1 在 DLBCL 中的功能和作用机制。CCK8 和 EdU 检测表明，β-TRCP1 可在 TNFα 的刺激下促进 DLBCL 细胞的生长。此外，过表达β-TRCP1 可增强 TNFα 存在时 NF-κB 的激活。此外，β-TRCP1 的异位表达降低了 IκB-α 的表达，但增加了磷酸化 p65 的表达。此外，β-TRCP1 通过加速 G1-S 期转变促进细胞周期进程。我们还发现，沉默β-TrCP1 增加了米托蒽醌诱导的细胞生长停滞和细胞凋亡。基于这些，我们提出β-TRCP1 的表达通过 TNF 依赖性 NF-κB 激活促进了 DLBCL 细胞的增殖。