m6A methylome in WT- and K177Q-METTL3 reconstituting MDA-MB-231 cells as well as in METTL3-deficient MDA-MB-231 cells.

We report the application of MeRIP sequencing technology for high-throughput profiling of m6A methylome in breast cancer cells. Comparison of m6A methylome between METTL3-WT and METTL3-K177Q reconstituting cells revealed the following findings: 1) Significant global alteration of methylation sites due to K177Q mutation (termed as KQ-m6A signature). 2) GO analysis of the differential m6A-MeRIP candidates enriched pathways involved in chromatin modification, RNA splicing, DNA damage, cell cycle, and autophagy, consistent with a critical role of m6A-mediated nuclear biological activities and highlighted generally recognized cellular events associated with tumorigenesis. 3) we dissected potential mechanistic clues explaining the attenuated invasive phenotype in METTL3K177Q reconstituting cells. Overall design: Examination of different m6A modification levels and gene expressions in WT- and K177Q-METTL3 reconstituting MDA-MB-231 cells as well as in METTL3-deficient MDA-MB-231 cells.