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题目:: M-CSF from Cancer Cells Induces Fatty Acid Synthase and PPARβ/δ Activation in Tumor Myeloid Cells, Leading to Tumor Progression.
作者:: Park(Jonghanne),Lee(Sang Eun),Hur(Jin),Hong(Eun Byeol),Choi(Jae-Il),Yang(Ji-Min),Kim(Ju-Young),Kim(Young-Chan),Cho(Hyun-Jai),Peters(Jeffrey M),Ryoo(Seung-Bum),Kim(Young Tae),Kim(Hyo-Soo)
状态:: 发布时间2015-03-10 , 更新时间 2015-03-11
期刊:: Cell Rep
摘要:: We investigate crosstalk between cancer cells and stromal myeloid cells. We find that Lewis lung carcinoma cells significantly induce PPARβ/δ activity in myeloid cells in vitro and in vivo. Myeloid cell-specific knockout of PPARβ/δ results in impaired growth of implanted tumors, and this is restored by adoptive transfer of wild-type myeloid cells. We find that IL-10 is a downstream effector of PPARβ/δ and facilitates tumor cell invasion and angiogenesis. This observation is supported by the finding that the CD11bIL-10 pro-tumoral myeloid cell is scarcely detected in tumors from myeloid-cell-specific PPARβ/δ knockout mice, where vessel densities are also decreased. Fatty acid synthase (FASN) is shown to be an upstream regulator of PPARβ/δ in myeloid cells and is induced by M-CSF secreted from tumor cells. Our study gives insight into how cancer cells influence myeloid stromal cells to get a pro-tumoral phenotype.
语言:: eng
DOI:: 10.1016/j.celrep.2015.02.024

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