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本帖最后由 饶冠华 于 2011-4-12 12:08 编辑 / _/ O: N; { D; x6 J- H* M# ?, \
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CCL18 from Tumor-Associated Macrophages Promotes Breast Cancer Metastasis via PITPNM3, G) x1 _7 i9 @; g- t2 w, [
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 S. Anderson, Qiang Liu, Mark E. Ewen, Xuebiao Yao, Erwei SongSee AffiliationsHint: Rollover Authors and Affiliations Breast Tumor Center, Sun-Yat-Sen Memorial Hospital, Sun-Yat-Sen University, Guangzhou 510120, China/ v. C l: x$ [- g* j+ ~8 m! O
Department of Medical Oncology, No. 2 Affiliated Hospital, Guangzhou Medical College, Guangzhou 510260, China
% K7 Z% A/ `3 e5 P Anhui Key Laboratory for Cellular Dynamics & Chemical Biology, Hefei National Laboratory for Physical Sciences at Nanoscale, and University of Science & Technology of China, Hefei, Anhui 230027, China4 ?# r: q& w/ Y* ~' Y, y
Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA
9 [/ ^0 R% K V( z. A3 m Corresponding author& A4 C, L3 o$ _0 W; d- n; K
These authors contributed equally to this work V3 \- J& @" ]- k7 d* L
! m3 j- f# R' w! XTumor-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.
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