| Literature DB >> 24373972 |
Justin D Lathia1, Meizhang Li2, Maksim Sinyuk3, Alvaro G Alvarado4, William A Flavahan5, Kevin Stoltz3, Ann Mari Rosager6, James Hale3, Masahiro Hitomi4, Joseph Gallagher7, Qiulian Wu7, Jody Martin8, Jason G Vidal8, Ichiro Nakano9, Rikke H Dahlrot10, Steinbjørn Hansen10, Roger E McLendon11, Andrew E Sloan12, Shideng Bao13, Anita B Hjelmeland13, Christian T Carson8, Ulhas P Naik14, Bjarne Kristensen6, Jeremy N Rich15.
Abstract
Stem cells reside in niches that regulate the balance between self-renewal and differentiation. The identity of a stem cell is linked with the ability to interact with its niche through adhesion mechanisms. To identify targets that disrupt cancer stem cell (CSC) adhesion, we performed a flow cytometry screen on patient-derived glioblastoma (GBM) cells and identified junctional adhesion molecule A (JAM-A) as a CSC adhesion mechanism essential for self-renewal and tumor growth. JAM-A was dispensable for normal neural stem/progenitor cell (NPC) function, and JAM-A expression was reduced in normal brain versus GBM. Targeting JAM-A compromised the self-renewal of CSCs. JAM-A expression negatively correlated to GBM patient prognosis. Our results demonstrate that GBM-targeting strategies can be identified through screening adhesion receptors and JAM-A represents a mechanism for niche-driven CSC maintenance.Entities:
Mesh：
Substances：
Year: 2013 PMID： 24373972 PMCID： PMC3899718 DOI： 10.1016/j.celrep.2013.11.043
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423