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ELTD1 facilitates glioma proliferation, migration and invasion by activating JAK/STAT3/HIF-1α signaling axis
- Source :
- Scientific Reports, Vol 9, Iss 1, Pp 1-12 (2019), Scientific Reports
- Publication Year :
- 2019
- Publisher :
- Springer Science and Business Media LLC, 2019.
-
Abstract
- The upregulation of ELTD1 ([epidermal growth factor (EGF), latrophilin and seven transmembrane domain-containing 1] on chromosome 1) in tumor cells has been reported in several types of cancer and correlates with poor cancer prognosis. However, the role of ELTD1 in glioma progression remains unknown. In this study, we examined ELTD1 expression levels in human glioma cell lines and in sixteen human gliomas of different grades. The molecular effects of ELTD1 in glioma cells were measured using quantitative polymerase chain reaction (qRT-PCR), Western blotting, Cell proliferation assays, Matrigel migration and invasion assays and brain orthotopic xenografts. We found that high expression levels of ELTD1 were positively associated with cancer progression and poor prognosis in human glioma. Mechanistically, ELTD1 activated the JAK/STAT3/HIF-1α signaling axis and p-STAT3 bound with HIF-1α. Taken together, our data provide a plausible mechanism for ELTD1-modulated glioma progression and suggest that ELTD1 may represent a potential therapeutic target in the prevention and therapy of glioma.
- Subjects :
- Adult
Male
STAT3 Transcription Factor
lcsh:Medicine
Biology
Article
Receptors, G-Protein-Coupled
Cell growth
Downregulation and upregulation
Cell Movement
Epidermal growth factor
Cell Line, Tumor
Glioma
medicine
Humans
Cell migration
lcsh:Science
STAT3
Cell Proliferation
Janus Kinases
Matrigel
Multidisciplinary
Brain Neoplasms
lcsh:R
Cancer
Hypoxia-Inducible Factor 1, alpha Subunit
Prognosis
medicine.disease
CNS cancer
Gene Expression Regulation, Neoplastic
Real-time polymerase chain reaction
Disease Progression
Cancer research
biology.protein
Female
lcsh:Q
Signal Transduction
Subjects
Details
- ISSN :
- 20452322
- Volume :
- 9
- Database :
- OpenAIRE
- Journal :
- Scientific Reports
- Accession number :
- edsair.doi.dedup.....34c392762c173920f4373979c729289c