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Meg3 Induces EMT and Invasion of Glioma Cells via Autophagy
- Source :
- OncoTargets and Therapy. 13:989-1000
- Publication Year :
- 2020
- Publisher :
- Informa UK Limited, 2020.
-
Abstract
- Background Glioma is one of the most common malignant tumors. Glioblastoma (grade IV) is considered the most malignant form of human brain tumors. Maternal expression gene 3 (Meg3) encodes a non-coding RNA (ncRNA) that plays an important role in the development and progression of cancer. However, the role of Meg3 in glioma cells remains largely unclear. Methods Reverse transcription-quantitative (RT-q) PCR was conducted to evaluate the mRNA expression related to cell autophagy and EMT while protein expression was detected by Western blotting. Staining of acidic vacuoles and immunofluorescence staining were used to detect autophagy. The ability of cells to migrate and invade was detected by Transwell migration and invasion assays. Results In the present study, it was found that the overexpression of Meg3 induced EMT, migration and invasion of glioma cells, whereas Meg3 overexpression induced autophagy of glioma cells. More importantly, the inhibition of autophagy impaired the EMT of glioma cells. In addition, Meg3-induced EMT, migration and invasion could be partially reversed by autophagy inhibitors, chloroquine (CQ) and Lys05, in glioma cells. Conclusion All data suggest that Meg3 induces EMT and invasion of glioma cells via autophagy. Overall, the findings of the present study demonstrate the importance of Meg3 in the molecular etiology of glioma, which also indicate its potential applications in the treatment of glioma.
- Subjects :
- 0301 basic medicine
MEG3
Autophagy
Cell
Cancer
Vacuole
Biology
medicine.disease
Blot
03 medical and health sciences
030104 developmental biology
0302 clinical medicine
medicine.anatomical_structure
Oncology
030220 oncology & carcinogenesis
Glioma
Gene expression
medicine
Cancer research
Pharmacology (medical)
Subjects
Details
- ISSN :
- 11786930
- Volume :
- 13
- Database :
- OpenAIRE
- Journal :
- OncoTargets and Therapy
- Accession number :
- edsair.doi...........223acfb0be9fcf31c29b47c374c24f21