Abstract
Background Numerous lncRNAs were found as regulatory factors for occurrence and progression of various tumors, but there is still less research on the role of lncRNAs in malignant progression of glioma. Methods Bioinformatics analysis analyzed differential genes (DEGs) in the TCGA database. MTT, flow cytometry, and Transwell assays were performed to test the proliferation, apoptosis, migration, and invasion of cells. qRT-PCR and western blot were conducted to detect RNA and protein expressions of each gene, respectively. CHIP assay verified the binding relationship between genes. FISH assayed subcellar location of CRNDE, and xenograft in nude mice was performed for in vivo verification. Results CRNDE was upregulated in glioma cells, and overexpression of CRNDE facilitated malignant progression of glioma cells. CRNDE regulated occurrence and development of glioma through the CRNDE-ETS1-GPR17 axis. ETS1 was proved to target promoter region of GPR17. Overexpression of CRNDE promoted the binding between ETS1 and the promoter region of GPR17, thus, promoting the transcription of GPR17, while silencing of GPR17 inhibited promotion of CRNDE on proliferation, migration, and invasion of glioma cells. Conclusions These results demonstrated that CRNDE regulated GPR17 expression by binding ETS1, a transcription factor, thereby affecting glioma development. The results also indicated that CRNDE could serve as a possible therapeutic target and prognostic biomarker for glioma.
Highlights
Glioma is an aggressive primary brain tumor, which is featured as invasive growth and early metastasis [1]
By analyzing the expression differences of these 5 lncRNAs in normal samples and glioma tumor samples of GSE60161 chip, CRNDE was significantly upregulated in tumor samples (Figure 1(b)), and the difference was the most significant when compared with the normal samples (∣logFC ∣ = 4:342887) (Table S4)
The results were that CRNDE was markedly highly expressed in all 4 glioma cell lines when compared to HEB cells (Figure 1(d)). These results displayed that CRNDE was upregulated in glioma cells
Summary
Glioma is an aggressive primary brain tumor, which is featured as invasive growth and early metastasis [1]. Radiotherapy, chemotherapy, and targeted therapy have developed in recent decades, the treatment of glioma, especially GBM, is still not satisfactory [3]. MTT, flow cytometry, and Transwell assays were performed to test the proliferation, apoptosis, migration, and invasion of cells. CHIP assay verified the binding relationship between genes. CRNDE regulated occurrence and development of glioma through the CRNDE-ETS1-GPR17 axis. ETS1 was proved to target promoter region of GPR17. Overexpression of CRNDE promoted the binding between ETS1 and the promoter region of GPR17, promoting the transcription of GPR17, while silencing of GPR17 inhibited promotion of CRNDE on proliferation, migration, and invasion of glioma cells. These results demonstrated that CRNDE regulated GPR17 expression by binding ETS1, a transcription factor, thereby affecting glioma development. The results indicated that CRNDE could serve as a possible therapeutic target and prognostic biomarker for glioma
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