Ceacam1L Modulates STAT3 Signaling to Control the Proliferation of Glioblastoma-Initiating Cells
Copyright policy )Ceacam1L Modulates STAT3 Signaling to Control the Proliferation of Glioblastoma-Initiating Cells
Abstract Glioblastoma-initiating cells (GIC) are a tumorigenic cell subpopulation resistant to radiotherapy and chemotherapy, and are a likely source of recurrence. However, the basis through which GICs are maintained has yet to be elucidated in detail. We herein demonstrated that the carcinoembryonic antigen–related cell adhesion molecule Ceacam1L acts as a crucial factor in GIC maintenance and tumorigenesis by activating c-Src/STAT3 signaling. Furthermore, we showed that monomers of the cytoplasmic domain of Ceacam1L bound to c-Src and STAT3 and induced their phosphorylation, whereas oligomerization of this domain ablated this function. Our results suggest that Ceacam1L-dependent adhesion between GIC and surrounding cells play an essential role in GIC maintenance and proliferation, as mediated by signals transmitted by monomeric forms of the Ceacam1L cytoplasmic domain. Cancer Res; 75(19); 4224–34. ©2015 AACR.
- Hokkaido Bunkyo University Japan
- RIKEN Japan
- Kumamoto University Japan
- Hokkaido University Japan
- Ehime University Japan
Neovascularization, Pathologic, Brain Neoplasms, Gene Expression Profiling, Kaplan-Meier Estimate, Astrocytoma, Carcinoembryonic Antigen, Neoplasm Proteins, Polymerization, CSK Tyrosine-Protein Kinase, Mice, Antigens, CD, Biomarkers, Tumor, Neoplastic Stem Cells, Animals, Humans, Cell Self Renewal, Phosphorylation, Glioblastoma, Cell Adhesion Molecules, Cell Division
Neovascularization, Pathologic, Brain Neoplasms, Gene Expression Profiling, Kaplan-Meier Estimate, Astrocytoma, Carcinoembryonic Antigen, Neoplasm Proteins, Polymerization, CSK Tyrosine-Protein Kinase, Mice, Antigens, CD, Biomarkers, Tumor, Neoplastic Stem Cells, Animals, Humans, Cell Self Renewal, Phosphorylation, Glioblastoma, Cell Adhesion Molecules, Cell Division
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