期刊
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
卷 9, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fcell.2021.658757
关键词
MSC; tumor associated MSC; retinoic acid; interleukin-17; interferon-γ tumor microenvironment
资金
- National Key Research and Development Program of China [2017YFA0103403, 2018YFA0107200]
- Key Research and Development Program of Guangdong Province [2019B020234002]
- NSFC [81822001, 81900101, 81800164, 81870127, 82000838, 31871467]
- Shenzhen Foundation of Science and Technology [JCYJ20170818103626421, JCYJ20190806164009212]
- National Science and Technology Major Project of China [2017YFA0105500]
- Guangdong Innovative and Entrepreneurial Research Team Program [2016ZT06S029, 2019ZT08Y485]
- Sanming Project of Medicine in Shenzhen [SZSM201911004]
- 111 Project [B13037]
This study found that interleukin 17 (IL-17) cooperating with interferon gamma can transform bone marrow mesenchymal stem/stromal cells (BMSCs) into tumor-associated MSCs (TA-MSCs), promoting tumor progression. Retinoic acid inhibits the NF-κB signaling pathway to regulate the function of TA-MSCs and inhibit tumor growth.
Bone marrow mesenchymal stem/stromal cells (BMSCs) can be transformed into tumor-associated MSCs (TA-MSCs) within the tumor microenvironment to facilitate tumor progression. However, the underline mechanism and potential therapeutic strategy remain unclear. Here, we explored that interleukin 17 (IL-17) cooperating with IFN gamma transforms BMSCs into TA-MSCs, which promotes tumor progression by recruiting macrophages/monocytes and myeloid-derived suppressor cells (MDSCs) in murine melanoma. IL-17 and IFN gamma transformed TA-MSCs have high expression levels of myelocyte-recruiting chemokines (CCL2, CCL5, CCL7, and CCL20) mediated by activated NF-kappa B signaling pathway. Furthermore, retinoic acid inhibits NF-kappa B signaling, decreases chemokine expression, and suppresses the tumor-promoting function of transformed TA-MSCs by prohibiting the recruitment of macrophages/monocytes and MDSCs in the tumor microenvironment. Overall, our findings demonstrate that IL-17 collaborating with IFN gamma to induce TA-MSC transformation, which can be targeted by RA for melanoma treatment.
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