| Literature DB >> 33863879 |
Takashi Nishina1, Yutaka Deguchi2, Daisuke Ohshima3, Wakami Takeda2,4, Masato Ohtsuka5,6, Shigeyuki Shichino7, Satoshi Ueha7, Soh Yamazaki2, Mika Kawauchi2, Eri Nakamura8, Chiharu Nishiyama4, Yuko Kojima9, Satomi Adachi-Akahane3, Mizuho Hasegawa10, Mizuho Nakayama11, Masanobu Oshima11, Hideo Yagita12, Kazutoshi Shibuya13, Tetuo Mikami14, Naohiro Inohara10, Kouji Matsushima7, Norihiro Tada8, Hiroyasu Nakano15,16.
Abstract
Interleukin (IL)-11 is a member of the IL-6 family of cytokines and is involved in multiple cellular responses, including tumor development. However, the origin and functions of IL-11-producing (IL-11+) cells are not fully understood. To characterize IL-11+ cells in vivo, we generate Il11 reporter mice. IL-11+ cells appear in the colon in murine tumor and acute colitis models. Il11ra1 or Il11 deletion attenuates the development of colitis-associated colorectal cancer. IL-11+ cells express fibroblast markers and genes associated with cell proliferation and tissue repair. IL-11 induces the activation of colonic fibroblasts and epithelial cells through phosphorylation of STAT3. Human cancer database analysis reveals that the expression of genes enriched in IL-11+ fibroblasts is elevated in human colorectal cancer and correlated with reduced recurrence-free survival. IL-11+ fibroblasts activate both tumor cells and fibroblasts via secretion of IL-11, thereby constituting a feed-forward loop between tumor cells and fibroblasts in the tumor microenvironment.Entities:
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Year: 2021 PMID： 33863879 DOI： 10.1038/s41467-021-22450-3
Source DB: PubMed Journal: Nat Commun ISSN： 2041-1723 Impact factor: 14.919