The Embryonic Key Pluripotent Factor NANOG Mediates Glioblastoma Cell Migration via the SDF1/CXCR4 Pathway

NANOG is a key transcription factor required for maintaining pluripotency of embryonic stem cells. Elevated NANOG expression levels have been reported in many types of human cancers, including lung, oral, prostate, stomach, breast, and brain. Several studies reported the correlation between NANOG ex...

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Published inInternational journal of molecular sciences Vol. 22; no. 19; p. 10620
Main Authors Sánchez-Sánchez, Ana Virginia, García-España, Antonio, Sánchez-Gómez, Pilar, Font-de-Mora, Jaime, Merino, Marián, Mullor, José Luis
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 01.10.2021
MDPI
Subjects
Binding sites
Brain cancer
Breast
cancer cell migration
cancer stem cell
Cell adhesion & migration
Chemokine receptors
Chemokines
CXCR4
CXCR4 protein
Embryo cells
Embryos
Evolutionary conservation
Gene expression
Genotype & phenotype
Glioblastoma
Glioblastoma cells
Metastases
Motility
NANOG
Pluripotency
Prostate
Regulatory sequences
SDF-1 protein
Stem cells
Therapeutic targets
Transcription factors
Tumors
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Summary:NANOG is a key transcription factor required for maintaining pluripotency of embryonic stem cells. Elevated NANOG expression levels have been reported in many types of human cancers, including lung, oral, prostate, stomach, breast, and brain. Several studies reported the correlation between NANOG expression and tumor metastasis, revealing itself as a powerful biomarker of poor prognosis. However, how NANOG regulates tumor progression is still not known. We previously showed in medaka fish that Nanog regulates primordial germ cell migration through Cxcr4b, a chemokine receptor known for its ability to promote migration and metastasis in human cancers. Therefore, we investigated the role of human NANOG in CXCR4-mediated cancer cell migration. Of note, we found that NANOG regulatory elements in the CXCR4 promoter are functionally conserved in medaka fish and humans, suggesting an evolutionary conserved regulatory axis. Moreover, CXCR4 expression requires NANOG in human glioblastoma cells. In addition, transwell assays demonstrated that NANOG regulates cancer cell migration through the SDF1/CXCR4 pathway. Altogether, our results uncover NANOG-CXCR4 as a novel pathway controlling cellular migration and support Nanog as a potential therapeutic target in the treatment of Nanog-dependent tumor progression.
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ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms221910620