Purpose: Differentially expressed long non-coding ribonucleic acids (lncRNAs) have been reported as a key factor of glioma carcinogenesis, but the underlying mechanism involved is still unknown.
Materials and methods: In the present study, lncRNA HOXC13 antisense RNA (HOXC13-AS) was identified as a potential oncogene in glioma, and Western blotting, wound healing and Transwell assays were carried out to explore the effects of HOXC13-AS on the epithelial-mesenchymal transition (EMT) process as well as the migration and invasion of glioma cells.
Results: A further mechanistic study showed that HOXC13-AS sponged miR-122-5p to indirectly regulate SATB1 expression and affect the EMT process via the Wnt/β-catenin pathway. Meanwhile, the promoter activity was significantly increased via c-Myc, a key factor of the Wnt/β-catenin pathway, thus forming a positive HOXC13-AS-miR-122-5p-SATB1-c-Myc feedback loop to drive the malignant behavior in glioma.
Discussion: This study evidences the constitutive HOXC13-AS-miR-122-5p-SATB1-c-Myc feedback loop and provides a potential therapeutic target for glioma treatment.
Keywords: HOXC13-AS, epithelial-mesenchymal transition, competing endogenous RNA, miR-122-5p, glioma