S1PR1-STAT3 Signaling Is Crucial for Myeloid Cell Colonization at Future Metastatic Sites

被引：297

作者：

Deng, Jiehui ^{[1
]}

Liu, Yong ^{[1
]}

Lee, Heehyoung ^{[1
]}

Herrmann, Andreas ^{[1
]}

Zhang, Wang ^{[1
]}

Zhang, Chunyan ^{[1
]}

Shen, Shudan ^{[1
]}

Priceman, Saul J. ^{[1
]}

Kujawski, Maciej ^{[1
]}

Pal, Sumanta K. ^{[2
]}

Raubitschek, Andrew ^{[1
]}

Hoon, Dave S. B. ^{[6
]}

Forman, Stephen ^{[3
]}

Figlin, Robert A. ^{[7
]}

Liu, Jie ^{[8
,9
]}

Jove, Richard ^{[4
,5
]}

Yu, Hua ^{[1
,9
]}

机构：

[1] City Hope Natl Med Ctr, Beckman Res Inst, Dept Canc Immunotherapeut & Tumor Immunol, Duarte, CA 91010 USA

[2] City Hope Natl Med Ctr, Beckman Res Inst, Dept Med Oncol, Duarte, CA 91010 USA

[3] City Hope Natl Med Ctr, Beckman Res Inst, Dept Hematol & Hematopoiet Cell Transplant, Duarte, CA 91010 USA

[4] City Hope Natl Med Ctr, Beckman Res Inst, Dept Mol Med, Duarte, CA 91010 USA

[5] City Hope Comprehens Canc Ctr, Duarte, CA 91010 USA

[6] John Wayne Canc Inst, Dept Mol Oncol, Santa Monica, CA 90404 USA

[7] Cedars Sinai Med Ctr, Dept Hematol Oncol, Los Angeles, CA 90048 USA

[8] Fudan Univ, Shanghai Med Sch, Dept Immunol, Dept Digest Dis Huashan Hosp, Shanghai 200040, Peoples R China

[9] Ctr Translat Med, Shanghai 201203, Peoples R China

来源：

CANCER CELL | 2012年 / 21卷 / 05期

基金：

中国国家自然科学基金;

关键词：

PROMOTE TUMOR-GROWTH; STAT3; ACTIVATION; IMMUNE CELLS; ANGIOGENESIS; CANCER; PROGRESSION; RECRUITMENT; EXPRESSION; RECEPTOR; INFLAMMATION;

D O I：

10.1016/j.ccr.2012.03.039

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

Recent studies underscore the importance of myeloid cells in rendering distant organs hospitable for disseminating tumor cells to colonize. However, what enables myeloid cells to have an apparently superior capacity to colonize distant organs is unclear. Here, we show that S1PR1-STAT3 upregulation in tumor cells induces factors that activate S1PR1-STAT3 in various cells in premetastatic sites, leading to premetastatic niche formation. Targeting either S1PR1 or STAT3 in myeloid cells disrupts existing premetastatic niches. S1PR1-STAT3 pathway enables myeloid cells to intravasate, prime the distant organ microenvironment and mediate sustained proliferation and survival of their own and other stromal cells at future metastatic sites. Analyzing tumor-free lymph nodes from cancer patients shows elevated myeloid infiltrates, STAT3 activity, and increased survival signal.

引用

页码：642 / 654

页数：13

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