M-CSF from cancer cells induces fatty acid synthase and PPARβ/δ activation in tumor myeloid cells, leading to tumor progression

Jonghanne Park; Sang Eun Lee; Jin Hur; Eun Byeol Hong; Jae Il Choi; Ji Min Yang; Ju Young Kim; Young Chan Kim; Hyun Jai Cho; Jeffrey M. Peters; Seung Bum Ryoo; Young Tae Kim; Hyo Soo Kim

doi:10.1016/j.celrep.2015.02.024

M-CSF from cancer cells induces fatty acid synthase and PPARβ/δ activation in tumor myeloid cells, leading to tumor progression

Jonghanne Park
, Sang Eun Lee
, Jin Hur
, Eun Byeol Hong
, Jae Il Choi
, Ji Min Yang
, Ju Young Kim
, Young Chan Kim
, Hyun Jai Cho
, Jeffrey M. Peters
, Seung Bum Ryoo
, Young Tae Kim
, Hyo Soo Kim

Research output: Contribution to journal › Article › peer-review

84 Scopus citations

Abstract

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 invitro and invivo. 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 CD11b^lowIL-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.

Original language	English (US)
Pages (from-to)	1614-1625
Number of pages	12
Journal	Cell Reports
Volume	10
Issue number	9
DOIs	https://doi.org/10.1016/j.celrep.2015.02.024
State	Published - Mar 10 2015

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

All Science Journal Classification (ASJC) codes

General Biochemistry, Genetics and Molecular Biology

Access to Document

10.1016/j.celrep.2015.02.024

Cite this

Park, J., Lee, S. E., Hur, J., Hong, E. B., Choi, J. I., Yang, J. M., Kim, J. Y., Kim, Y. C., Cho, H. J., Peters, J. M., Ryoo, S. B., Kim, Y. T., & Kim, H. S. (2015). M-CSF from cancer cells induces fatty acid synthase and PPARβ/δ activation in tumor myeloid cells, leading to tumor progression. Cell Reports, 10(9), 1614-1625. https://doi.org/10.1016/j.celrep.2015.02.024

@article{519c68d0556c49ada18e4e4a2f45974b,

title = "M-CSF from cancer cells induces fatty acid synthase and PPARβ/δ activation in tumor myeloid cells, leading to tumor progression",

abstract = "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 invitro and invivo. 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 CD11blowIL-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.",

author = "Jonghanne Park and Lee, \{Sang Eun\} and Jin Hur and Hong, \{Eun Byeol\} and Choi, \{Jae Il\} and Yang, \{Ji Min\} and Kim, \{Ju Young\} and Kim, \{Young Chan\} and Cho, \{Hyun Jai\} and Peters, \{Jeffrey M.\} and Ryoo, \{Seung Bum\} and Kim, \{Young Tae\} and Kim, \{Hyo Soo\}",

note = "Funding Information: We thank Ms. H.W. Jung for her excellent assistance in animal experiments. This study was supported by grants from the Bio \& Medical Technology Development Program (2010-0020258) of Korea National Research Foundation (NRF); the Innovative Research Institute for Cell Therapy (A062260) funded by Ministry of Health \& Welfare (MHW); and the Korea Health Technology R\&D Project (HI12C16910000, HI14C1277, and HI12C0199) through the Korea Health Industry Development Institute, funded by MHW. Publisher Copyright: {\textcopyright} 2015 The Authors.",

year = "2015",

month = mar,

day = "10",

doi = "10.1016/j.celrep.2015.02.024",

language = "English (US)",

volume = "10",

pages = "1614--1625",

journal = "Cell Reports",

issn = "2211-1247",

publisher = "Elsevier BV",

number = "9",

}

TY - JOUR

T1 - M-CSF from cancer cells induces fatty acid synthase and PPARβ/δ activation in tumor myeloid cells, leading to tumor progression

AU - Park, Jonghanne

AU - Lee, Sang Eun

AU - Hur, Jin

AU - Hong, Eun Byeol

AU - Choi, Jae Il

AU - Yang, Ji Min

AU - Kim, Ju Young

AU - Kim, Young Chan

AU - Cho, Hyun Jai

AU - Peters, Jeffrey M.

AU - Ryoo, Seung Bum

AU - Kim, Young Tae

AU - Kim, Hyo Soo

N1 - Funding Information: We thank Ms. H.W. Jung for her excellent assistance in animal experiments. This study was supported by grants from the Bio & Medical Technology Development Program (2010-0020258) of Korea National Research Foundation (NRF); the Innovative Research Institute for Cell Therapy (A062260) funded by Ministry of Health & Welfare (MHW); and the Korea Health Technology R&D Project (HI12C16910000, HI14C1277, and HI12C0199) through the Korea Health Industry Development Institute, funded by MHW. Publisher Copyright: © 2015 The Authors.

PY - 2015/3/10

Y1 - 2015/3/10

N2 - 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 invitro and invivo. 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 CD11blowIL-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.

AB - 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 invitro and invivo. 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 CD11blowIL-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.

UR - https://www.scopus.com/pages/publications/84924599857

UR - https://www.scopus.com/pages/publications/84924599857#tab=citedBy

U2 - 10.1016/j.celrep.2015.02.024

DO - 10.1016/j.celrep.2015.02.024

M3 - Article

C2 - 25753425

AN - SCOPUS:84924599857

SN - 2211-1247

VL - 10

SP - 1614

EP - 1625

JO - Cell Reports

JF - Cell Reports

IS - 9

ER -

M-CSF from cancer cells induces fatty acid synthase and PPARβ/δ activation in tumor myeloid cells, leading to tumor progression

Abstract

UN SDGs

All Science Journal Classification (ASJC) codes

Access to Document

Other files and links

Fingerprint

Cite this