Abstract
Homeobox (HOX) genes, including HOXA13, are involved in human cancer. We found that HOXA13 expression was associated with glioma grade and prognosis. Bioinformatics analysis revealed that most of the HOXA13-associated genes were enriched in cancer-related signaling pathways and mainly involved in the regulation of transcription. We transfected four glioma cell lines with Lenti-si HOXA13. HOXA13 increased cell proliferation and invasion and inhibited apoptosis. HOXA13 decreased β-catenin, phospho-smad2, and phospho-smad3 in the nucleus and increased phospho-β-catenin in the cytoplasm. Furthermore, downregulation of HOXA13 in orthotopic tumors decreased tumor growth. We suggest that HOXA13 promotes glioma progression in part via Wnt- and TGF-β-induced EMT and is a potential diagnostic biomarker for glioblastoma and an independent prognostic factor in high-grade glioma.
Highlights
The Homeobox genes (Hox genes), which were firstly discovered in Drosophila, are characterized by the existence of a recognizable 183-base pair DNA sequence that encodes a highly conserved 61-amino acid peptide known as the homeodomain [1]
In order to explore the role of the 5′ HOXA genes in gliomas, we first measured the expression of HOXA9, HOXA10, HOXA11, and HOXA13 protein in 66 gliomas specimens of different grades
By western-blot analysis, HOXA9, HOXA11, and HOXA13 were dramatically up-regulated in glioblastoma multiforme (GBM), and HOXA10 merely showed a slight increase in high-grade glioma (Figure 2A)
Summary
The Homeobox genes (Hox genes), which were firstly discovered in Drosophila, are characterized by the existence of a recognizable 183-base pair DNA sequence that encodes a highly conserved 61-amino acid peptide known as the homeodomain [1]. Abnormal expression of HOX genes is associated with disease progression and predicts outcome. Our previous research demonstrated that HOTAIR (HOX transcript antisense RNA), a noncoding RNA at the distal tip of the HOXC cluster, is a negative prognostic factor for glioma patients and that its expression could promote cell cycle progression in gliomas as a result of the binding of its 5′ domain to the PRC2 complex [14, 15]. A substantial body of scientific evidence indicates that the expression of HOX genes that are critical for normal embryonic development is aberrant in and contributes to carcinogenesis
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