BST-2/Tetherin is involved in BAFF-enhanced proliferation and survival via canonical NF-κB signaling in neoplastic B-lymphoid cells
BST-2/Tetherin is involved in BAFF-enhanced proliferation and survival via canonical NF-κB signaling in neoplastic B-lymphoid cells
复制标题
BST-2/Tetherin 通过肿瘤 B 淋巴细胞中的典型 NF-κB 信号传导参与 BAFF 增强的增殖和存活
DOI：
10.1016/j.yexcr.2020.112399
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发表时间：
2021-01-01
影响因子：
3.7
通讯作者：
Zheng, Lingyan
中科院分区：
文献类型：
--
作者：
Fu, Jiayao;Shi, Huan;Zheng, Lingyan
干燥综合征（SS）的发展伴随着B细胞过度增殖和突变。我们先前的研究鉴定了BST-2（也称为Tetherin/CD 317）在来自外周血或浸润的唾液腺的B细胞中的异常表达。然而，BST-2在调节B细胞活化中的作用仍然未知。在这项研究中，我们确定BST-2可以响应BAFF模拟，但不响应肿瘤B细胞系中的其他B细胞模拟物。CCK-8测定、EdU测定和膜联蛋白V/PI染色表明，BST-2抑制减弱了Raji细胞和Daudi细胞中BAFF增强的增殖和存活。在肿瘤性B淋巴细胞中筛选BAFF相关信号表明BST-2参与BAFF刺激后NF-κ B信号的调节。然而，在正常和BAFF模拟条件下，JSH-23抑制NF-κ B显著降低Raji和Daudi细胞的增殖和存活。总的来说，我们的研究结果表明，BST-2/Tetherin是一个BAFF响应膜因子参与调节NF-κ B信号，从而有助于增殖和肿瘤B淋巴细胞的生存。我们的研究提供了一个潜在的分子机制异常过度激活的B细胞后SS的发展。
The development of Sjogren's syndrome (SS) is accompanied by B cell hyperproliferation and mutation. Our previous study identified aberrant expression of BST-2 (also known as Tetherin/CD317) in B cells from either the peripheral blood or infiltrated salivary glands. However, the roles of BST-2 in the regulation of B cell activation remain unknown. In this study, we identified that BST-2 can respond to BAFF simulation but not to other B cell simulators in neoplastic B cell lines. A CCK-8 assay, an EdU assay and Annexin V/PI staining indicated that BST-2 inhibition attenuated BAFF-enhanced proliferation and survival in both Raji cells and Daudi cells. Screening of BAFF-related signaling in neoplastic B-lymphoid cells indicated that BST-2 was involved in the regulation of NF-kappa B signaling upon BAFF simulation. However, inhibition of NF-kappa B by JSH-23 significantly reduced the proliferation and survival of Raji and Daudi cells under both normal and BAFF-simulated conditions. Collectively, our results indicate that BST-2/Tetherin is a BAFF-responsive membrane factor involved in the regulation of NF-kappa B signaling, thereby assisting in the proliferation and survival of neoplastic B-lymphoid cells. Our study provides a potential molecular mechanism underlying aberrant overactivation of B cells upon SS development.