Title |
Regulation of CXCR4/AKT-signaling-induced cell invasion and tumor metastasis by RhoA, Rac-1, and Cdc42 in human esophageal cancer
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Published in |
Tumor Biology, December 2015
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DOI | 10.1007/s13277-015-4504-x |
Pubmed ID | |
Authors |
Jing Guo, Xiaofang Yu, Jie Gu, Zongwu Lin, Guangyin Zhao, Fengkai Xu, Chunlai Lu, Di Ge |
Abstract |
CXC chemokines and their cognate receptors have been implicated wildly in cancer pathogenesis. In the present study, we report a critical cause relationship between CXCR4 expression and tumorigenesis in the setting of human esophageal squamous cell carcinoma (ESCC). In ESCC cells, CXCR4 expression was significantly higher than in human esophageal epithelial cells (HEEC). Reduction of CXCR4 in ESCC cells reduced cell proliferation and invasion in vitro and tumor growth in vivo. Among the potential downstream targets of CXCR4-CXCL12 are RhoA, Rac-1, and Cdc42, which are likely to contribute to the invasiveness of ESCC cells. Finally, we found that CXCR4-CXCL12/AKT axis regulates RhoA, Rac-1, and Cdc42 to modulate cell invasion and tumor metastasis. Together, these results demonstrate a role for CXCR4 in ESCC metastasis and progression and suggest potential targets for therapeutic intervention. |
X Demographics
Geographical breakdown
Country | Count | As % |
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Unknown | 1 | 100% |
Demographic breakdown
Type | Count | As % |
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Members of the public | 1 | 100% |
Mendeley readers
Geographical breakdown
Country | Count | As % |
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Unknown | 10 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
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Student > Ph. D. Student | 3 | 30% |
Lecturer | 2 | 20% |
Student > Bachelor | 2 | 20% |
Professor | 1 | 10% |
Student > Doctoral Student | 1 | 10% |
Other | 0 | 0% |
Unknown | 1 | 10% |
Readers by discipline | Count | As % |
---|---|---|
Medicine and Dentistry | 2 | 20% |
Biochemistry, Genetics and Molecular Biology | 2 | 20% |
Agricultural and Biological Sciences | 2 | 20% |
Pharmacology, Toxicology and Pharmaceutical Science | 1 | 10% |
Nursing and Health Professions | 1 | 10% |
Other | 0 | 0% |
Unknown | 2 | 20% |