start-ver=1.4
cd-journal=joma
no-vol=44
cd-vols=
no-issue=7
article-no=
start-page=910
end-page=919
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=202107
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=PC3-secreted microprotein is expressed in glioblastoma stem-like cells and human glioma tissues
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Glioblastoma multiforme (GBM) is the most prevalent malignant primary brain tumor with a high recurrence rate. Despite multimodal therapy including surgical resection, chemotherapy, and radiotherapy, the median survival time after the initial diagnosis of GBM is approximately 14 months. Since cancer stem cells (CSCs) are considered the leading cause of cancer recurrence, glioblastoma stem cell-targeted therapy is a promising strategy for the treatment of GBM. However, because CSC heterogeneity has been implicated in the difficulties of CSC-target therapy, more in-depth knowledge of CSC biology is still required to develop novel therapies. In this study, we established single cell-derived tumorspheres from human glioblastoma U87MG cells. One of these tumorspheres, P4E8 clone, showed CSC-like phenotypes, such as self-renewal capacity, expression of CSC markers, resistance to anti-cancer agents, and in vivo tumorigenicity. Therefore, we used P4E8 cells as a cell-based model of glioblastoma stem cells (GSCs). Gene expression analysis using microarray indicated that the most highly expressed genes in P4E8 cells compared to the parental U87MG were PC3-secreted microprotein (MSMP). Furthermore, MSMP was expressed in patient-derived GSCs and human glioma tissues at the protein level, implying that MSMP might contribute to glioma development and progression.
en-copyright=
kn-copyright=

en-aut-name=MaruyamaMasato
en-aut-sei=Maruyama
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=NakanoYousuke
en-aut-sei=Nakano
en-aut-mei=Yousuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=NishimuraTakuya
en-aut-sei=Nishimura
en-aut-mei=Takuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IwataRyoichi
en-aut-sei=Iwata
en-aut-mei=Ryoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=MatsudaSatoshi
en-aut-sei=Matsuda
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=HayashiMikio
en-aut-sei=Hayashi
en-aut-mei=Mikio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=NakaiYuki
en-aut-sei=Nakai
en-aut-mei=Yuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=NonakaMasahiro
en-aut-sei=Nonaka
en-aut-mei=Masahiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=SugimotoTetsuo
en-aut-sei=Sugimoto
en-aut-mei=Tetsuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Anatomy and Brain Science, Kansai Medical University
kn-affil=

affil-num=2
en-affil=Department of Anatomy and Brain Science, Kansai Medical University
kn-affil=

affil-num=3
en-affil=Department of Anatomy and Brain Science, Kansai Medical University
kn-affil=

affil-num=4
en-affil=Department of Neurosurgery, Kansai Medical University
kn-affil=

affil-num=5
en-affil=Department of Cell Signaling, Institute of Biomedical Science, Kansai Medical University
kn-affil=

affil-num=6
en-affil=Department of Physiology, Kansai Medical University
kn-affil=

affil-num=7
en-affil=Department of Anatomy and Brain Science, Kansai Medical University
kn-affil=

affil-num=8
en-affil=Department of Neurosurgery, Kansai Medical University
kn-affil=

affil-num=9
en-affil=Department of Anatomy and Brain Science, Kansai Medical University
kn-affil=
END