期刊
CANCER CELL
卷 23, 期 2, 页码 171-185出版社
CELL PRESS
DOI: 10.1016/j.ccr.2012.12.021
关键词
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资金
- National Institutes of Health (NIH) Cancer Center support grant [CA016672]
- NIH [T32CA009599, R01CA157880]
- Department of Defense [CA100879]
- William C. Liedtke, Jr., Chair in Cancer Research
- R.E. Bob Smith Fellowship
We report a paracrine effect whereby endothelial cells (ECs) promote the cancer stem cell (CSC) phenotype of human colorectal cancer (CRC) cells. We showed that, without direct cell-cell contact, ECs secrete factors that promoted the CSC phenotype in CRC cells via Notch activation. In human CRC specimens, CD133 and Notch intracellular domain-positive CRC cells colocalized in perivascular regions. An EC-derived, soluble form of Jagged-1, via ADAM17 proteolytic activity, led to Notch activation in CRC cells in a paracrine manner; these effects were blocked by immunodepletion of Jagged-1 in EC-conditioned medium or blockade of ADAM17 activity. Collectively, ECs play an active role in promoting Notch signaling and the CSC phenotype by secreting soluble Jagged-1.
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