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Chemotherapy-Induced IL34 Enhances Immunosuppression by Tumor-Associated Macrophages and Mediates Survival of Chemoresistant Lung Cancer Cells

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Title: Chemotherapy-Induced IL34 Enhances Immunosuppression by Tumor-Associated Macrophages and Mediates Survival of Chemoresistant Lung Cancer Cells
Other Titles: An importance of IL-34 in cancer chemoresistance
Authors: Baghdadi, Muhammad Browse this author
Wada, Haruka Browse this author →KAKEN DB
Nakanishi, Sayaka Browse this author
Abe, Hirotake Browse this author
Han, Nanumi Browse this author
Putra, Wira Eka Browse this author
Endo, Daisuke Browse this author
Watari, Hidemichi Browse this author →KAKEN DB
Sakuragi, Noriaki Browse this author →KAKEN DB
Hida, Yasuhiro Browse this author →KAKEN DB
Kaga, Kichizo Browse this author →KAKEN DB
Miyagi, Yohei Browse this author →KAKEN DB
Yokose, Tomoyuki Browse this author
Takano, Atsushi Browse this author →KAKEN DB
Daigo, Yataro Browse this author →KAKEN DB
Seino, Ken-ichiro Browse this author →KAKEN DB
Issue Date: Oct-2016
Publisher: American Association for Cancer Research
Journal Title: Cancer research
Volume: 76
Issue: 20
Start Page: 6030
End Page: 6042
Publisher DOI: 10.1158/0008-5472.CAN-16-1170
PMID: 27550451
Abstract: The ability of tumor cells to escape immune destruction and their acquired resistance to chemotherapy are major obstacles to effective cancer therapy. Although immune checkpoint therapies such as anti-PD-1 address these issues in part, clinical responses remain limited to a subpopulation of patients. In this report, we identified IL34 produced by cancer cells as a driver of chemoresistance. In particular, we found that IL34 modulated the functions of tumor-associated macrophages to enhance local immunosuppression and to promote the survival of chemoresistant cancer cells by activating AKT signaling. Targeting IL34 in chemoresistant tumors resulted in a remarkable inhibition of tumor growth when accompanied with chemotherapy. Our results define a pathogenic role for IL34 in mediating immunosuppression and chemoresistance and identify it as a tractable target for anticancer therapy.
Type: article (author version)
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 清野 研一郎

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