CXCR4 and cancer

被引：248

作者：

Furusato, Bungo ^{[1
,2
]}

Mohamed, Ahmed ^{[1
]}

Uhlen, Mathias ^{[3
]}

Rhim, Johng S. ^{[1
]}

机构：

[1] Uniformed Serv Univ Hlth Sci, Dept Surg, Ctr Prostate Dis Res, Bethesda, MD 20814 USA

[2] Armed Forces Inst Pathol, Dept Genitourinary Pathol, Washington, DC 20306 USA

[3] Royal Inst Technol KTH, AlbaNova Univ Ctr, Dept Biotechnol, Stockholm, Sweden

来源：

PATHOLOGY INTERNATIONAL | 2010年 / 60卷 / 07期

关键词：

cancer; cancer stem cell; CXCR4; gene fusion; CHEMOKINE RECEPTOR CXCR4; CELL LUNG-CANCER; LYMPH-NODE METASTASIS; ACUTE MYELOGENOUS LEUKEMIA; EPIDERMAL-GROWTH-FACTOR; ACUTE MYELOID-LEUKEMIA; HUMAN-MELANOMA CELLS; PROSTATE-CANCER; BREAST-CANCER; SQUAMOUS-CELL;

D O I：

10.1111/j.1440-1827.2010.02548.x

中图分类号：

R36 [病理学];

学科分类号：

100104 ;

摘要：

The chemokine receptor CXCR4 belongs to the large superfamily of G protein-coupled receptors and has been identified to play a crucial role in a number of biological processes, including the trafficking and homeostasis of immune cells such as T lymphocytes. CXCR4 has also been found to be a prognostic marker in various types of cancer, including leukemia and breast cancer, and recent evidence has highlighted the role of CXCR4 in prostate cancer. Furthermore, CXCR4 expression is upregulated in cancer metastasis, leading to enhanced signaling. These observations suggest that CXCR4 is important for the progression of cancer. The CXCR4-CXCL12 (stromal cell-derived factor 1 (SDF-1)) axis has additionally been identified to have a role in normal stem cell homing. Interestingly, cancer stem cells also express CXCR4, indicating that the CXCR4-SDF-1 axis may direct the trafficking and metastasis of these cells to organs that express high levels of SDF-1, such as the lymph nodes, lungs, liver, and bone. This review focuses on the current knowledge of CXCR4 regulation and how deregulation of this protein may contribute to the progression of cancer.

引用

页码：497 / 505

页数：9

共 154 条

[91] Defects of B-cell lymphopoiesis and bone-marrow myelopoiesis in mice lacking the CXC chemokine PBSF/SDF-1 [J].