Journal Article Ceacam1L Modulates STAT3 Signaling to Control the Proliferation of Glioblastoma-Initiating Cells
Ceacam1L as a new GIC regulator

Kaneko, Sadahiro  ,  Nakatani, Yuka  ,  Takezaki, Tatsuya  ,  Hide, Takuichiro  ,  Yamashita, Daisuke  ,  Ohtsu, Naoki  ,  Ohnishi, Takanori  ,  Terasaka, Shunsuke  ,  Houkin, Kiyohiro  ,  Kondo, Toru

75 ( 19 )  , pp.4224 - 4234 , 2015-10-01 , American Association for Cancer Research
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.

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