Cycling cancer persister cells arise from lineages with distinct programs.

ABSTRACT: Non-genetic mechanisms have recently emerged as important drivers of cancer therapy failure¹, where some cancer cells can enter a reversible drug-tolerant persister state in response to treatment². Although most cancer persisters remain arrested in the presence of the drug, a rare subset can re-enter the cell cycle under constitutive drug treatment. Little is known about the non-genetic mechanisms that enable cancer persisters to maintain proliferative capacity in the presence of drugs. To study this rare, transiently resistant, proliferative persister population, we developed Watermelon, a high-complexity expressed barcode lentiviral library for simultaneous tracing of each cell's clonal origin and proliferative and transcriptional states. Here we show that cycling a

SUBMITTER: Oren Y 

PROVIDER: S-EPMC9209846 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature