| First Author | Fu J | Year | 2021 |
| Journal | Exp Cell Res | Volume | 398 |
| Issue | 1 | Pages | 112399 |
| PubMed ID | 33245890 | Mgi Jnum | J:302121 |
| Mgi Id | MGI:6503306 | Doi | 10.1016/j.yexcr.2020.112399 |
| Citation | Fu J, et al. (2021) BST-2/Tetherin is involved in BAFF-enhanced proliferation and survival via canonical NF-kappaB signaling in neoplastic B-lymphoid cells. Exp Cell Res 398(1):112399 |
| abstractText | 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-kappaB signaling upon BAFF simulation. However, inhibition of NF-kappaB 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-kappaB 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. |
