Yang Zhihao, Bian Erbao, Xu Yadi, Ji Xinghu, Tang Feng, Ma Chunchun, Wang Hongliang, Zhao Bing
Department of Neurosurgery, The Second Affiliated Hospital of Anhui Medical University, Hefei 230601, People's Republic of China.
Cerebral Vascular Disease Research Center, Anhui Medical University, Hefei 230601, People's Republic of China.
Onco Targets Ther. 2020 Jan 31;13:989-1000. doi: 10.2147/OTT.S239648. eCollection 2020.
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.
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.
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.
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.
胶质瘤是最常见的恶性肿瘤之一。胶质母细胞瘤（IV级）被认为是人类脑肿瘤中最恶性的形式。母源表达基因3（Meg3）编码一种非编码RNA（ncRNA），其在癌症的发生和发展中起重要作用。然而，Meg3在胶质瘤细胞中的作用仍不清楚。
采用逆转录定量（RT-q）PCR评估与细胞自噬和上皮-间质转化（EMT）相关的mRNA表达，同时通过蛋白质印迹法检测蛋白质表达。采用酸性空泡染色和免疫荧光染色检测自噬。通过Transwell迁移和侵袭试验检测细胞的迁移和侵袭能力。
在本研究中，发现Meg3的过表达诱导胶质瘤细胞的EMT、迁移和侵袭，而Meg3过表达诱导胶质瘤细胞自噬。更重要的是，自噬的抑制损害了胶质瘤细胞的EMT。此外，自噬抑制剂氯喹（CQ）和Lys05可部分逆转Meg3诱导的胶质瘤细胞的EMT、迁移和侵袭。
所有数据表明，Meg3通过自噬诱导胶质瘤细胞的EMT和侵袭。总体而言，本研究结果证明了Meg3在胶质瘤分子病因学中的重要性，这也表明了其在胶质瘤治疗中的潜在应用。
