m6A Modification Suppresses Viral Mimicry in Colorectal Cancer by Inhibiting Double-stranded RNA Formation from Alu Repeats
We systematically investigated how METTL3 and its N6-methyladenosine (m6A) modification regulate dsRNA stress induced by dysregulated retroelements in cancer cells. Our findings reveal that not all cancer cells depend equally on METTL3 to evade viral mimicry responses. We identified the molecular mechanisms underlying this dependency and explored strategies to induce synthetic vulnerability using viral mimicry-inducing agents. Our results highlight METTL3 as a key player in enabling a subset of cancer cells to tolerate dsRNA stress, ultimately promoting their survival--a dependency that could be exploited for novel therapeutic interventions.