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Supplementary Material for: Membrane-Associated Kaposi Sarcoma-Associated Herpesvirus Glycoprotein B Promotes Cell Adhesion and Inhibits Migration of Cells via Upregulating IL-1β and TNF-α

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DataCite Commons2020-08-30 更新2024-08-17 收录
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https://karger.figshare.com/articles/Supplementary_Material_for_Membrane-Associated_Kaposi_Sarcoma-Associated_Herpesvirus_Glycoprotein_B_Promotes_Cell_Adhesion_and_Inhibits_Migration_of_Cells_via_Upregulating_IL-1_and_TNF-_/6061421
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<b><i>Objectives:</i></b> Kaposi sarcoma-associated herpesvirus (KSHV) glycoprotein B (gB) is expressed on the viral envelope as well as on the cytoplasmic membrane of infected cells. In the current study, we aimed to decipher the impact of membrane-associated gB on adhesion and migration of cells via modulating the expression of cytokines. <b><i>Methods:</i></b> A combination of polymerase chain reaction array, cell adhesion assay, and wound-healing migration assay was conducted to study the influence of the gB-induced cytokines on cell adhesion and migration. <b><i>Results:</i></b> Membrane-associated gB was demonstrated to significantly upregulate the expression of IL-1β and TNF-α. Elevated levels of these cytokines were observed in conditioned medium (CM) collected from gB-expressing cells (gB-CM) compared to CM collected from untransfected cells or cells transfected with empty vector. KSHV gB-induced IL-1β and TNF-α play a role in the ability of gB-CM to mediate cell adhesion while inhibiting migration. <b><i>Conclusion:</i></b> Our results provide novel evidence that demonstrates full-length gB expressed on cell membrane to mediate adhesion and inhibit migration of cells not only by autocrine mechanism mediated by RGD-based interactions [Hussein et al.: BMC Cancer 2016; 16: 148], but also by paracrine mechanism mediated by gB-induced IL-1β and TNF-α.
提供机构:
Karger Publishers
创建时间:
2018-03-29
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