期刊
CANCER CELL
卷 30, 期 4, 页码 533-547出版社
CELL PRESS
DOI: 10.1016/j.ccell.2016.09.003
关键词
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资金
- German Research Foundation (DFG) [FOR2314, SFB685]
- Gottfried Wilhelm Leibniz Program
- European Research Council
- German Ministry for Education and Research (BMBF)
- German Universities Excellence Initiative
- German Center for Translational Cancer Research (DKTK)
- German-Israeli Cooperation in Cancer Research (DKFZ-MOST)
- ERC
- Stiftung Experimentelle Biomedizin (Hofschneider Stiftung)
- Pre-clinical Comprehensive Center (PCCC)
- Helmholtz foundation
- Intramural Research Program of the NIH
- NCI
Oncogene-induced senescence causes hepatocytes to secrete cytokines, which induce their immune-mediated clearance to prevent tumor initiation, a process termed senescence surveillance. However, senescent hepatocytes give rise to hepatocellular carcinomas (HCCs), if the senescence program is bypassed or if senescent cells are not cleared. Here, we show context-specific roles for CCR2(+) myeloid cells in liver cancer. Senescence surveillance requires the recruitment and maturation of CCR2(+) myeloid cells, and CCR2 ablation caused outgrowth of HCC. In contrast, HCC cells block the maturation of recruited myeloid precursors, which, through NK cell inhibition, promote growth of murine HCC and worsen the prognosis and survival of human HCC patients. Thus, while senescent hepatocyte-secreted chemokines suppress liver cancer initiation, they may accelerate the growth of fully established HCC.
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