J-W Ji1, Y-D Zhang, Y-J Lai, C-G Huang. 1. Department of Neurosurgery, Changzheng Hospital Affiliated to Naval Military Medical University, Shanhai, P.R. China. naokeyisheng@163.com.
Abstract
OBJECTIVE: Methyltransferase-like 3 (Mettl3), one of "writers" for N6-methyladenosine RNA methylation is determined to participate in a variety of cell biological functions. However, the functions of Mettl3 on tumor growth of glioma remain unknown. Here, we conducted a research to explore the contribution of Mettl3 in the progression of glioma. PATIENTS AND METHODS: To detect the expression level of RNAs, quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed. To access the relative level of proteins, Western blot was conducted. The proliferative ability of glioma cells was detected by CCK-8 assay and colony formation assay. The migration and invasion of glioma cells were determined by wound healing assay and transwell invasion assay. RESULTS: The expression of Mettl3 was significantly downregulated in tumor tissues compared to the adjacent normal tissues. The downregulation of Mettl3 led to the enhancement of glioma cell proliferation, migration, and invasion in vitro, and promoted the tumor growth of glioma cells in vivo. In addition, further investigation confirmed that Mettl3 plays critical roles in the development of glioma by targeting PI3K/Akt pathway. CONCLUSIONS: Our study proves that Mettl3 plays a critical role in the proliferation, migration, and invasion of glioma cells by inactivating PI3K/Akt signaling pathway, providing a novel mechanism of glioma tumorigenesis and raising a new target for the treatment of glioma.
OBJECTIVE:Methyltransferase-like 3 (Mettl3), one of "writers" for N6-methyladenosine RNA methylation is determined to participate in a variety of cell biological functions. However, the functions of Mettl3 on tumor growth of glioma remain unknown. Here, we conducted a research to explore the contribution of Mettl3 in the progression of glioma. PATIENTS AND METHODS: To detect the expression level of RNAs, quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed. To access the relative level of proteins, Western blot was conducted. The proliferative ability of glioma cells was detected by CCK-8 assay and colony formation assay. The migration and invasion of glioma cells were determined by wound healing assay and transwell invasion assay. RESULTS: The expression of Mettl3 was significantly downregulated in tumor tissues compared to the adjacent normal tissues. The downregulation of Mettl3 led to the enhancement of glioma cell proliferation, migration, and invasion in vitro, and promoted the tumor growth of glioma cells in vivo. In addition, further investigation confirmed that Mettl3 plays critical roles in the development of glioma by targeting PI3K/Akt pathway. CONCLUSIONS: Our study proves that Mettl3 plays a critical role in the proliferation, migration, and invasion of glioma cells by inactivating PI3K/Akt signaling pathway, providing a novel mechanism of glioma tumorigenesis and raising a new target for the treatment of glioma.