School of Biosystems and Biomedical Sciences, College of Health Science, Korea University, Seoul 02841; Interdisciplinary Program in Precision Public Health, Korea University, Seoul 02841, Korea.
BMB Rep. 2022 Dec;55(12):602-608. doi: 10.5483/BMBRep.2022.55.12.161.
Uncontrolled chronic inflammation, in most cases due to excessive cytokine signaling through their receptors, is known to contribute to the development of tumorigenesis. Recently, it has been reported that the antiviral membrane protein interferon-induced transmembrane protein 3 (IFITM3), induced by interferon signaling as part of the inflammatory response after viral infection, contributes to the development of B-cell malignancy. The unexpected oncogenic signaling of IFITM3 upon malignant B cell activation elucidated the mechanism by which the uncontrolled expression of inflammatory proteins contributes to leukemogenesis. In this review, the potential effects of inflammatory cytokines on upregulation of IFITM3 and its contribution to tumorigenesis are discussed. [BMB Reports 2022; 55(12): 602-608].
失控的慢性炎症，在大多数情况下是由于细胞因子通过其受体过度信号传导，已知会导致肿瘤发生。最近有报道称，抗病毒膜蛋白干扰素诱导跨膜蛋白 3（IFITM3），作为病毒感染后炎症反应的一部分，由干扰素信号诱导，有助于 B 细胞恶性肿瘤的发展。IFITM3 在恶性 B 细胞激活时的意外致癌信号阐明了不受控制的炎症蛋白表达如何促进白血病发生的机制。在这篇综述中，讨论了炎症细胞因子对上调 IFITM3 的潜在影响及其对肿瘤发生的贡献。[BMB 报告 2022；55(12)：602-608]。
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