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Review
. 2022 Dec;55(12):602-608.
doi: 10.5483/BMBRep.2022.55.12.161.

Does IFITM3 link inflammation to tumorigenesis?

Jaewoong Lee  1
Affiliations
Review

Does IFITM3 link inflammation to tumorigenesis?

Jaewoong Lee. BMB Rep. 2022 Dec.

Abstract

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].

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Conflict of interest statement

CONFLICTS OF INTEREST

The authors have no conflicting interests.

Figures

Fig. 1
Fig. 1
Activated BCR signaling or its oncogenic mimics activate SRC family kinases such as LYN, resulting in phosphorylation of CD19-Y482/513 and IFITM3-Y20. Phosphorylated tyrosine residues on CD19, which provide docking sites for the SH2 domains of the PI3K regulatory subunit p85, facilitates localization and activation of PI3K to the lipid raft on plasma membrane. Transiently synthesized PIP3 by the PI3K catalytic subunit p110 stably accumulated by IFITM3 at the BCR signalosome. IFITM3, therefore, stabilizes the BCR signalosome, supports PIP3-mediated recruitment of downstream effector molecules such as BTK and ATK, enhances BCR signaling or BCR-mimicking oncogenic signaling. The effect of the amphipathic helix of IFITM3-mediated cholesterol accumulation at lipid raft on BCR signaling has not yet been investigated.
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References

    1. Xiong Y, Liu Y, Cao L, et al. Transcriptomic characteristics of bronchoalveolar lavage fluid and peripheral blood mononuclear cells in COVID-19 patients. Emerg Microbes Infect. 2020;9:761–770. doi: 10.1080/22221751.2020.1747363. - DOI - PMC - PubMed
    1. Fara A, Mitrev Z, Rosalia RA, et al. Cytokine storm and COVID-19, a chronicle of pro-inflammatory cytokines. Open Biol. 2020;10:200160. doi: 10.1098/rsob.200160.42f5a94ce41847c6b702ba38b44040c2 - DOI - PMC - PubMed
    1. Guo X, Steinkühler J, Marin M, et al. Interferon-induced transmembrane protein 3 blocks fusion of diverse enveloped viruses by altering mechanical properties of cell membranes. ACS Nano. 2021;15:8155–8170. doi: 10.1021/acsnano.0c10567. - DOI - PMC - PubMed
    1. Brodin P. Immune determinants of COVID-19 disease presentation and severity. Nat Med. 2021;27:28–33. doi: 10.1038/s41591-020-01202-8. - DOI - PubMed
    1. Greten FR, Grivennikov SI. Inflammation and cancer, triggers, mechanisms, and consequences. Immunity. 2019;51:27–41. doi: 10.1016/j.immuni.2019.06.025. - DOI - PMC - PubMed