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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.
Highlights
Glioma is the most prevalent tumor of CNS, and both the morbidity and mortality rates for gliomas have increased in recent years[1,2]
We found that the ELTD1 expression levels in the tumors were significantly higher than those in normal brains, especially in high-grade glioma (III + IV), by analyzing the bioinformatics data
We found that the ELTD1 expression levels were consistently upregulated in high-grade gliomas (III + IV)
Summary
Glioma is the most prevalent tumor of CNS (central nervous system), and both the morbidity and mortality rates for gliomas have increased in recent years[1,2]. ELTD1 includes a domain similar to EGF, a short cytoplasmic tail and a seven-trans-membrane domain[5]. It is reported for the first time that the function of ELTD1 is in postnatal cardiomyocytes and rat fetuses[5]. Dai S et al had proved that miR-139-5p inhibits tumor progression via targeting ELTD117. STAT3 has been shown to regulate HIF-1α19. Www.nature.com/scientificreports tumors and during tumor growth is significantly limited after knocking it out, which indicates that it exerts a vital role in cancer development[21,22,23]. In vitro and in vivo experiments have shown that ELTD1 exerts a vital role in facilitating glioma cells proliferation, migration, and invasion. Our results indicated that the JAK/STAT3/HIF-1α signaling may mediate this process
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