作者: Larisa Litovchick , Wenqi Wang , Sohee Jun , Jae-Il Park , Jae-Il Park
DOI: 10.1016/J.MOLCEL.2021.02.001
关键词:
摘要: The DREAM complex orchestrates cell quiescence and the cycle. However, how is deregulated in cancer remains elusive. Here, we report that PAF (PCLAF/KIAA0101) drives exit to promote lung tumorigenesis by remodeling complex. highly expressed adenocarcinoma (LUAD) associated with poor prognosis. Importantly, Paf knockout markedly suppressed LUAD development mouse models. depletion induced growth arrest. required for global expression of cell-cycle genes controlled repressive Mechanistically, inhibits formation binding RBBP4, a core subunit, leading transactivation target genes. Furthermore, pharmacological mimicking PAF-depleted transcriptomes inhibited tumor growth. Our results unveil PAF-remodeled bypasses suggest PAF-DREAM axis may be therapeutic vulnerability cancer.