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Ceacam1L Modulates STAT3 Signaling to Control the Proliferation of Glioblastoma-Initiating Cells
Title: | Ceacam1L Modulates STAT3 Signaling to Control the Proliferation of Glioblastoma-Initiating Cells |
Other Titles: | Ceacam1L as a new GIC regulator |
Authors: | Kaneko, Sadahiro Browse this author | Nakatani, Yuka Browse this author | Takezaki, Tatsuya Browse this author | Hide, Takuichiro Browse this author →KAKEN DB | Yamashita, Daisuke Browse this author | Ohtsu, Naoki Browse this author | Ohnishi, Takanori Browse this author →KAKEN DB | Terasaka, Shunsuke Browse this author →KAKEN DB | Houkin, Kiyohiro Browse this author →KAKEN DB | Kondo, Toru Browse this author →KAKEN DB |
Keywords: | Glioblastoma (GBM) | GBM-initiating cells (GICs) | Ceacam1L | c-Src | STAT3 |
Issue Date: | 1-Oct-2015 |
Publisher: | American Association for Cancer Research |
Journal Title: | Cancer research |
Volume: | 75 |
Issue: | 19 |
Start Page: | 4224 |
End Page: | 4234 |
Publisher DOI: | 10.1158/0008-5472.CAN-15-0412 |
PMID: | 26238781 |
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. |
Type: | article (author version) |
URI: | http://hdl.handle.net/2115/62923 |
Appears in Collections: | 遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 近藤 亨
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