Please use this identifier to cite or link to this item: https://ir.swu.ac.th/jspui/handle/123456789/13028
ชื่อเรื่อง: RUNX1 Regulates Migration, Invasion, and Angiogenesis via p38 MAPK Pathway in Human Glioblastoma
ผู้แต่ง: Sangpairoj K.
Vivithanaporn P.
Apisawetakan S.
Chongthammakun S.
Sobhon P.
Chaithirayanon K.
Keywords: gelatinase A
gelatinase B
interleukin 1beta
interstitial collagenase
mitogen activated protein kinase 14
small interfering RNA
transcription factor RUNX1
vasculotropin A
mitogen activated protein kinase p38
RUNX1 protein, human
transcription factor RUNX1
angiogenesis
Article
carcinogenesis
cell invasion
cell migration
controlled study
enzyme activation
gene expression
gene silencing
glioblastoma
glioblastoma cell line
human
human cell
in vitro study
MAPK signaling
priority journal
umbilical vein endothelial cell
brain tumor
cell motion
glioblastoma
metabolism
neovascularization (pathology)
pathology
physiology
tumor cell line
tumor invasion
Brain Neoplasms
Cell Line, Tumor
Cell Movement
Core Binding Factor Alpha 2 Subunit
Glioblastoma
Human Umbilical Vein Endothelial Cells
Humans
MAP Kinase Signaling System
Neoplasm Invasiveness
Neovascularization, Pathologic
p38 Mitogen-Activated Protein Kinases
วันที่เผยแพร่: 2017
บทคัดย่อ: Runt-related transcription factor 1 (RUNX1) is essential for the establishment of fetal and adult hematopoiesis and neuronal development. Aberrant expression of RUNX1 led to proliferation and metastasis of several cancers. The aim of the present study was to investigate the role of RUNX1 in migration, invasion, and angiogenesis of human glioblastoma using IL-1β-treated U-87 MG human glioblastoma cells as a model. IL-1β at 10 ng/ml stimulated translocation of RUNX1 into the nucleus with increased expressions of RUNX1, MMP-1, MMP-2, MMP-9, MMP-19, and VEGFA in U-87 MG cells. In addition, silencing of RUNX1 gene significantly suppressed U-87 MG cell migration and invasion abilities. Moreover, knockdown of RUNX1 mRNA in U-87 MG cells reduced the tube formation of human umbilical vein endothelial cells. Further investigation revealed that IL-1β-induced RUNX1 expression might be mediated via the p38 mitogen-activated protein kinase (MAPK) signaling molecule for the expression of these invasion- and angiogenic-related molecules. Together with an inhibitor of p38 MAPK (SB203580) could decrease RUNX1 mRNA expression. Thus, RUNX1 may be one of the putative molecular targeted therapies against glioma metastasis and angiogenesis through the activation of p38 MAPK signaling pathway. © 2016, Springer Science+Business Media New York.
URI: https://ir.swu.ac.th/jspui/handle/123456789/13028
https://www.scopus.com/inward/record.uri?eid=2-s2.0-85007236818&doi=10.1007%2fs10571-016-0456-y&partnerID=40&md5=0b8347fcd86f97f765d206fb82357f9d
ISSN: 2724340
Appears in Collections:Scopus 1983-2021

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