A KRAS-responsive long non-coding RNA controls microRNA processing

Abstract Wild-type KRAS ( WT ) amplification has been shown to be a secondary means of activation in cancer and associated with poor survival. Nevertheless, the precise role overexpression lung progression is largely unexplored. Here, we identify characterize KRAS-responsive lncRNA, KIMAT1 (ENSG00000228709) show that it correlates levels both cell lines specimens. Mechanistically, MYC target drives tumorigenesis by promoting processing oncogenic microRNAs (miRNAs) through DHX9 NPM1 stabilization while halting biogenesis miRNAs tumor suppressor function via MYC-dependent silencing p21, component Microprocessor Complex. knockdown suppresses not only expression but also downstream signaling, thereby arresting growth vitro vivo. Taken together, this study uncovers for maintaining positive feedback loop sustains signaling during provides proof principle interfering could strategy hamper KRAS-induced tumorigenesis.