TY - JOUR
T1 - Autophagy-dependent regulation of tumor metastasis by myeloid cells
AU - Jinushi, Masahisa
AU - Morita, Tomoko
AU - Xu, Zhihang
AU - Kinoshita, Ichiro
AU - Dosaka-Akita, Hirotoshi
AU - Yagita, Hideo
AU - Kawakami, Yutaka
N1 - Funding Information:
We thank Dr. N. Mizushima (University of Tokyo) for Atg-5 mice and LC3-GFP transgenic mice, and Mr. M. Baghdadi, Mr. A. Yoneda, Mr. S. Chiba and Ms. K. Kudo (Hokkaido University) for technical assistance. This study is partially supported by a Grant-in-Aid for Scientific Research and Scientific Research for Innovative Areas from the Ministry of Education, Culture, Sports, Science and Technology (MEXT) and the Ministry of Health, Labor and Welfare (M. J.). The authors declare no conflicts of interest in this study. flox/flox
Publisher Copyright:
© 2017 Jinushi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2017/7
Y1 - 2017/7
N2 - Autophagy is a vital process controlling the lysosomal degradation of cellular organelles and thereby regulating tissue homeostasis in an environment-dependent fashion. Recent studies have unveiled the critical role of tumor cell-derived autophagy in regulating pro-tumor and anti-tumor processes depending on different stages and tumor microenvironments. However, the precise mechanism whereby autophagy regulates tumor progression remains largely unclear. Since myeloid cells contribute to tumor progression and metastasis, we evaluated the role of myeloid cell-specific autophagy in the regulation of tumor progression. We found that the number and size of metastatic lesions were smaller in myeloid cell-specific autophagy-deficient mice. Furthermore, autophagy-mediated regulation of TGF-β in myeloid cells was associated with the induction of epithelial-mesenchymal transition (EMT), which increases the invasive and metastatic potentials of tumor cells. Myeloid-derived autophagy also plays a critical role in impairing antitumor immune responses and promoting the survival and accumulation of M2 macrophages in tumor tissues in a CSF-1 and TGF-β-dependent manner. Taken together, our findings elucidate previously unrecognized mechanisms by which myeloid cells promote tumor progression through autophagy-mediated regulation of malignancy and immune tolerance.
AB - Autophagy is a vital process controlling the lysosomal degradation of cellular organelles and thereby regulating tissue homeostasis in an environment-dependent fashion. Recent studies have unveiled the critical role of tumor cell-derived autophagy in regulating pro-tumor and anti-tumor processes depending on different stages and tumor microenvironments. However, the precise mechanism whereby autophagy regulates tumor progression remains largely unclear. Since myeloid cells contribute to tumor progression and metastasis, we evaluated the role of myeloid cell-specific autophagy in the regulation of tumor progression. We found that the number and size of metastatic lesions were smaller in myeloid cell-specific autophagy-deficient mice. Furthermore, autophagy-mediated regulation of TGF-β in myeloid cells was associated with the induction of epithelial-mesenchymal transition (EMT), which increases the invasive and metastatic potentials of tumor cells. Myeloid-derived autophagy also plays a critical role in impairing antitumor immune responses and promoting the survival and accumulation of M2 macrophages in tumor tissues in a CSF-1 and TGF-β-dependent manner. Taken together, our findings elucidate previously unrecognized mechanisms by which myeloid cells promote tumor progression through autophagy-mediated regulation of malignancy and immune tolerance.
UR - http://www.scopus.com/inward/record.url?scp=85022207181&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85022207181&partnerID=8YFLogxK
U2 - 10.1371/journal.pone.0179357
DO - 10.1371/journal.pone.0179357
M3 - Article
C2 - 28686632
AN - SCOPUS:85022207181
SN - 1932-6203
VL - 12
JO - PloS one
JF - PloS one
IS - 7
M1 - e0179357
ER -