CCL18 from Tumor-Associated Macrophages Promotes Breast Cancer Metastasis via PITPNM3

Jingqi Chen, Yandan Yao, Chang Gong, Fengyan Yu, Shicheng Su, Jianing Chen, Bodu Liu, Hui Deng, Fengsong Wang, Ling Lin, Herui Yao, Fengxi Su, Karen Anderson, Qiang Liu, Mark E. Ewen, Xuebiao Yao, Erwei Song

Research output: Contribution to journalArticle

252 Citations (Scopus)

Abstract

Tumor-associated macrophages (TAMs) can influence cancer progression and metastasis, but the mechanism remains unclear. Here, we show that breast TAMs abundantly produce CCL18, and its expression in blood or cancer stroma is associated with metastasis and reduced patient survival. CCL18 released by breast TAMs promotes the invasiveness of cancer cells by triggering integrin clustering and enhancing their adherence to extracellular matrix. Furthermore, we identify PITPNM3 as a functional receptor for CCL18 that mediates CCL18 effect and activates intracellular calcium signaling. CCL18 promotes the invasion and metastasis of breast cancer xenografts, whereas suppressing PITPNM3 abrogates these effects. These findings indicate that CCL18 derived from TAMs plays a critical role in promoting breast cancer metastasis via its receptor, PITPNM3.

Original languageEnglish (US)
Pages (from-to)541-555
Number of pages15
JournalCancer Cell
Volume19
Issue number4
DOIs
StatePublished - Apr 12 2011
Externally publishedYes

Fingerprint

Macrophages
Breast Neoplasms
Neoplasm Metastasis
Neoplasms
Calcium Signaling
Heterografts
Integrins
Extracellular Matrix
Cluster Analysis
Survival

ASJC Scopus subject areas

  • Cancer Research
  • Cell Biology
  • Oncology

Cite this

Chen, J., Yao, Y., Gong, C., Yu, F., Su, S., Chen, J., ... Song, E. (2011). CCL18 from Tumor-Associated Macrophages Promotes Breast Cancer Metastasis via PITPNM3. Cancer Cell, 19(4), 541-555. https://doi.org/10.1016/j.ccr.2011.02.006

CCL18 from Tumor-Associated Macrophages Promotes Breast Cancer Metastasis via PITPNM3. / Chen, Jingqi; Yao, Yandan; Gong, Chang; Yu, Fengyan; Su, Shicheng; Chen, Jianing; Liu, Bodu; Deng, Hui; Wang, Fengsong; Lin, Ling; Yao, Herui; Su, Fengxi; Anderson, Karen; Liu, Qiang; Ewen, Mark E.; Yao, Xuebiao; Song, Erwei.

In: Cancer Cell, Vol. 19, No. 4, 12.04.2011, p. 541-555.

Research output: Contribution to journalArticle

Chen, J, Yao, Y, Gong, C, Yu, F, Su, S, Chen, J, Liu, B, Deng, H, Wang, F, Lin, L, Yao, H, Su, F, Anderson, K, Liu, Q, Ewen, ME, Yao, X & Song, E 2011, 'CCL18 from Tumor-Associated Macrophages Promotes Breast Cancer Metastasis via PITPNM3', Cancer Cell, vol. 19, no. 4, pp. 541-555. https://doi.org/10.1016/j.ccr.2011.02.006
Chen, Jingqi ; Yao, Yandan ; Gong, Chang ; Yu, Fengyan ; Su, Shicheng ; Chen, Jianing ; Liu, Bodu ; Deng, Hui ; Wang, Fengsong ; Lin, Ling ; Yao, Herui ; Su, Fengxi ; Anderson, Karen ; Liu, Qiang ; Ewen, Mark E. ; Yao, Xuebiao ; Song, Erwei. / CCL18 from Tumor-Associated Macrophages Promotes Breast Cancer Metastasis via PITPNM3. In: Cancer Cell. 2011 ; Vol. 19, No. 4. pp. 541-555.
@article{ee7c4aca811e4919a124455cc954a506,
title = "CCL18 from Tumor-Associated Macrophages Promotes Breast Cancer Metastasis via PITPNM3",
abstract = "Tumor-associated macrophages (TAMs) can influence cancer progression and metastasis, but the mechanism remains unclear. Here, we show that breast TAMs abundantly produce CCL18, and its expression in blood or cancer stroma is associated with metastasis and reduced patient survival. CCL18 released by breast TAMs promotes the invasiveness of cancer cells by triggering integrin clustering and enhancing their adherence to extracellular matrix. Furthermore, we identify PITPNM3 as a functional receptor for CCL18 that mediates CCL18 effect and activates intracellular calcium signaling. CCL18 promotes the invasion and metastasis of breast cancer xenografts, whereas suppressing PITPNM3 abrogates these effects. These findings indicate that CCL18 derived from TAMs plays a critical role in promoting breast cancer metastasis via its receptor, PITPNM3.",
author = "Jingqi Chen and Yandan Yao and Chang Gong and Fengyan Yu and Shicheng Su and Jianing Chen and Bodu Liu and Hui Deng and Fengsong Wang and Ling Lin and Herui Yao and Fengxi Su and Karen Anderson and Qiang Liu and Ewen, {Mark E.} and Xuebiao Yao and Erwei Song",
year = "2011",
month = "4",
day = "12",
doi = "10.1016/j.ccr.2011.02.006",
language = "English (US)",
volume = "19",
pages = "541--555",
journal = "Cancer Cell",
issn = "1535-6108",
publisher = "Cell Press",
number = "4",

}

TY - JOUR

T1 - CCL18 from Tumor-Associated Macrophages Promotes Breast Cancer Metastasis via PITPNM3

AU - Chen, Jingqi

AU - Yao, Yandan

AU - Gong, Chang

AU - Yu, Fengyan

AU - Su, Shicheng

AU - Chen, Jianing

AU - Liu, Bodu

AU - Deng, Hui

AU - Wang, Fengsong

AU - Lin, Ling

AU - Yao, Herui

AU - Su, Fengxi

AU - Anderson, Karen

AU - Liu, Qiang

AU - Ewen, Mark E.

AU - Yao, Xuebiao

AU - Song, Erwei

PY - 2011/4/12

Y1 - 2011/4/12

N2 - Tumor-associated macrophages (TAMs) can influence cancer progression and metastasis, but the mechanism remains unclear. Here, we show that breast TAMs abundantly produce CCL18, and its expression in blood or cancer stroma is associated with metastasis and reduced patient survival. CCL18 released by breast TAMs promotes the invasiveness of cancer cells by triggering integrin clustering and enhancing their adherence to extracellular matrix. Furthermore, we identify PITPNM3 as a functional receptor for CCL18 that mediates CCL18 effect and activates intracellular calcium signaling. CCL18 promotes the invasion and metastasis of breast cancer xenografts, whereas suppressing PITPNM3 abrogates these effects. These findings indicate that CCL18 derived from TAMs plays a critical role in promoting breast cancer metastasis via its receptor, PITPNM3.

AB - Tumor-associated macrophages (TAMs) can influence cancer progression and metastasis, but the mechanism remains unclear. Here, we show that breast TAMs abundantly produce CCL18, and its expression in blood or cancer stroma is associated with metastasis and reduced patient survival. CCL18 released by breast TAMs promotes the invasiveness of cancer cells by triggering integrin clustering and enhancing their adherence to extracellular matrix. Furthermore, we identify PITPNM3 as a functional receptor for CCL18 that mediates CCL18 effect and activates intracellular calcium signaling. CCL18 promotes the invasion and metastasis of breast cancer xenografts, whereas suppressing PITPNM3 abrogates these effects. These findings indicate that CCL18 derived from TAMs plays a critical role in promoting breast cancer metastasis via its receptor, PITPNM3.

UR - http://www.scopus.com/inward/record.url?scp=79953747613&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79953747613&partnerID=8YFLogxK

U2 - 10.1016/j.ccr.2011.02.006

DO - 10.1016/j.ccr.2011.02.006

M3 - Article

VL - 19

SP - 541

EP - 555

JO - Cancer Cell

JF - Cancer Cell

SN - 1535-6108

IS - 4

ER -