lncRNA CHROMR promotes DLBCL viability and invasion in an m ⁶A-dependent manner

Long noncoding RNA (lncRNA) CHROMR is closely associated with the development of diffuse large B-cell lymphoma (DLBCL) and drug resistance to rituximab. However, the mechanism underlying the upregulation of the lncRNA CHROMR in DLBCL cells remains unknown. N ⁶-methyladenosine (m ⁶A) modifications are involved in the tumorigenesis and progression of numerous human cancers. This study reveals that m ⁶A complexes are enriched on the lncRNA CHROMR in DLBCL cells, as determined by methylated RNA immunoprecipitation-quantitative polymerase chain reaction (MeRIP-qPCR) assay and bioinformatics analysis. Our results demonstrate that methyltransferase-like 3 (METTL3) acts as the m ⁶A methylation writer for the lncRNA CHROMR at site 3 ("UGGAACUU"), while insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) functions as the reader of this modification. Together, they enhance the stability of the lncRNA CHROMR. Furthermore, both METTL3 and IGF2BP1 play critical roles in regulating the viability and invasion of DLBCL cells. These findings highlight the indispensable role of m ⁶A modification in the lncRNA CHROMR, revealing METTL3 and IGF2BP1 as epigenetic mediators that regulate CHROMR expression.