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Ceacam1L Modulates STAT3 Signaling to Control the Proliferation of Glioblastoma-Initiating Cells

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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)
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)
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)

Submitter: 近藤 亨

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