FTO negatively regulates the cytotoxic activity of natural killer cells
- Authors
- Kim, S.-M.[Kim, S.-M.]; Oh, S.-C.[Oh, S.-C.]; Lee, S.-Y.[Lee, S.-Y.]; Kong, L.-Z.[Kong, L.-Z.]; Lee, J.-H.[Lee, J.-H.]; Kim, T.-D.[Kim, T.-D.]
- Issue Date
- 5-Apr-2023
- Publisher
- John Wiley and Sons Inc
- Keywords
- epitranscriptome; FTO; m< sup> 6< /sup> A regulator; N6-methyladenosine; NK cell
- Citation
- EMBO Reports, v.24, no.4
- Indexed
- SCIE
SCOPUS
- Journal Title
- EMBO Reports
- Volume
- 24
- Number
- 4
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/103387
- DOI
- 10.15252/embr.202255681
- ISSN
- 1469-221X
- Abstract
- N6-Methyladenosine (m6A) is the most abundant epitranscriptomic mark and plays a fundamental role in almost every aspect of mRNA metabolism. Although m6A writers and readers have been widely studied, the roles of m6A erasers are not well-understood. Here, we investigate the role of FTO, one of the m6A erasers, in natural killer (NK) cell immunity. We observe that FTO-deficient NK cells are hyperactivated. Fto knockout (Fto−/−) mouse NK cells prevent melanoma metastasis in vivo, and FTO-deficient human NK cells enhance the antitumor response against leukemia in vitro. We find that FTO negatively regulates IL-2/15-driven JAK/STAT signaling by increasing the mRNA stability of suppressor of cytokine signaling protein (SOCS) family genes. Our results suggest that FTO is an essential modulator of NK cell immunity, providing a new immunotherapeutic strategy for allogeneic NK cell therapies. © 2023 The Authors.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - Pharmacy > Department of Pharmacy > 1. Journal Articles
![qrcode](https://api.qrserver.com/v1/create-qr-code/?size=55x55&data=https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/103387)
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.