Crosstalk between GBM cells and mesenchymal stemlike cells promotes the invasiveness of GBM through the C5a/p38/ZEB1 axis
- Authors
- Lim, Eun-Jung; Kim, Seungmo; Oh, Yoonjee; Suh, Yongjoon; Kaushik, Neha; Lee, Ji-Hyun; Lee, Hae-June; Kim, Min-Jung; Park, Myung-Jin; Kim, Rae-Kwon; Cha, Junghwa; Kim, Se Hoon; Shim, Jin-Kyoung; Choi, Junjeong; Chang, Jong Hee; Hong, Yong Kil; Huh, Yong Min; Kim, Pilnam; Kang, Seok-Gu; Lee, Su-Jae
- Issue Date
- Oct-2020
- Publisher
- OXFORD UNIV PRESS INC
- Keywords
- C5a; glioblastoma; invasiveness; mesenchymal stem-like cells; tumor microenvironment
- Citation
- NEURO-ONCOLOGY, v.22, no.10, pp.1452 - 1462
- Indexed
- SCIE
SCOPUS
- Journal Title
- NEURO-ONCOLOGY
- Volume
- 22
- Number
- 10
- Start Page
- 1452
- End Page
- 1462
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/1739
- DOI
- 10.1093/neuonc/noaa064
- ISSN
- 1522-8517
- Abstract
- Background
Mesenchymal stemlike cells (MSLCs) have been detected in many types of cancer including brain tumors and have received attention as stromal cells in the tumor microenvironment. However, the cellular mechanisms underlying their participation in cancer progression remain largely unexplored. The aim of this study was to determine whether MSLCs have a tumorigenic role in brain tumors.
Methods
To figure out molecular and cellular mechanisms in glioma invasion, we have cultured glioma with MSLCs in a co-culture system.
Results
Here, we show that MSLCs in human glioblastoma (GBM) secrete complement component C5a, which is known for its role as a complement factor. MSLC-secreted C5a increases expression of zinc finger E-box-binding homeobox 1 (ZEB1) via activation of p38 mitogen-activated protein kinase (MAPK) in GBM cells, thereby enhancing the invasion of GBM cells into parenchymal brain tissue.
Conclusion
Our results reveal a mechanism by which MSLCs undergo crosstalk with GBM cells through the C5a/p38 MAPK/ZEB1 signaling loop and act as a booster in GBM progression.
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