Table 1.

Examples of tumour-suppressor vs. oncogenic roles of N⁶-methyladenosine (m⁶A) in glioblastoma, inferred from the study of specific factors involved in m⁶A modulation. NMD: nonsense-mediated decay; n.a.: not determined.

Factor Involved in m6A RNA Modification	Mediator/Target Molecules	Cell or Tissue Model	Inferred Tumorigenic vs Tumour-Suppressor Role of m6A RNA Methylation	Ref.
METTL3	n.a.	Glioma tissues and cell lines	Tumour-suppressor	[38]
METTL3 and METTL14	several oncogenes, whose expression increased upon METTL3 or METTL14 depletion	Glioblastoma stem cells	Tumour-suppressor	[39]
ALKBH5	FOXM1, HuR, FOXM1-AS	Glioblastoma stem cells and tissues	Tumour-suppressor	[41]
ALKBH5	n.a.	One glioblastoma cell line	Tumour-suppressor	[43]
FTO	MYC and other oncogenes	Glioma cell lines	Tumour- suppressor	[36]
WTAP	n.a.	Glioma tissues	Oncogenic	[46]
METTL3	SOX2, HuR	Glioblastoma stem cells	Oncogenic	[48]
METTL3	Several aspects of coding and noncoding RNA metabolism (splicing, editing)	One glioblastoma stem cell line	Oncogenic	[49]
METTL3 and YTHDC1	Modulation of NMD of mRNAs for splicing factors SRSF3, SRSF6, and SRSF11	Glioblastoma stem cells and U87 glioblastoma cell line	Oncogenic	[50]