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M-CSF from Cancer Cells Induces Fatty Acid Synthase and PPARβ/δ Activation in Tumor Myeloid Cells, Leading to Tumor Progression
암 세포의 대식세포 콜로니 자극인자를 통한 골수성 세포의 지방산합성효소 및 PPARβ/δ 핵수용체 활성화에 따른 종양 성장의 기전

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Authors
박종한
Advisor
김효수
Major
의과대학 의과학과
Issue Date
2016-02
Publisher
서울대학교 대학원
Keywords
Tumor MicroenvironmentMyeloid CellsPPAR deltaInterleukin-10Fatty Acid Synthases
Description
학위논문 (박사)-- 서울대학교 대학원 : 의과대학 의과학과, 2016. 2. 김효수.
Abstract
Introduction: Tumor myeloid cells have a central role in tumor progression. However, the mechanism by which the myeloid cells sense the tumor microenvironment and activate their pro-tumoral function remains unclear.
Methods: Lewis lung carcinoma tumor model with PPARβ/δ-deficient bone marrow transplantation and adoptive transfer of wild-type macrophages were used to study the role of myeloid PPARβ/δ in tumor progression.
Results: PPARβ/δ is strongly expressed and activated in tumor myeloid cells. PPARβ/δ promotes tumor growth and angiogenesis by inducing pro-tumoral phenotype of myeloid cells. This pro-tumoral phenotype, represented as IL-10 expression, stimulates tumor cell invasion and angiogenesis apart from its well-known immune regulatory function.
Conclusions: The activation of PPARβ/δ in myeloid cell is dependent on increased fatty acid synthase expression, which is augmented by cancer cell derived cytokine, M-CSF.
Language
English
URI
https://hdl.handle.net/10371/122307
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College of Medicine/School of Medicine (의과대학/대학원)Dept. of Biomedical Sciences (대학원 의과학과)Theses (Ph.D. / Sc.D._의과학과)
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