학술논문
The KDM5A/RBP2 histone demethylase represses NOTCH signaling to sustain neuroendocrine differentiation and promote small cell lung cancer tumorigenesis
Document Type
Article
Author
Oser, Matthew G.; Sabet, Amin H.; Gao, Wenhua; Chakraborty, Abhishek A.; Schinzel, Anna C.; Jennings, Rebecca B.; Fonseca, Raquel; Bonal, Dennis M.; Booker, Matthew A.; Flaifel, Abdallah; Novak, Jesse S.; Christensen, Camilla L.; Zhang, Hua; Herbert, Zachary T.; Tolstorukov, Michael Y.; Buss, Elizabeth J.; Wong, Kwok-Kin; Bronson, Roderick T.; Nguyen, Quang-De; Signoretti, Sabina; Kaelin, William G.
Source
Genes & Development; 2019, Vol. 33 Issue: 23-24 p1718-1738, 21p
Subject
Language
ISSN
08909369; 15495477
Abstract
In this study from Oser et al., the authors investigated how RB1 loss causes a neuroendocrine phenotype in different tumor types. They show that histone demethylase KDM5A (also known as RBP2 or JARID1A) promotes small cell lung cancer (SCLC) proliferation and SCLCs neuroendocrine differentiation phenotype through sustained expression of the neuroendocrine transcription factor ASCL1 by repressing NOTCH2 and NOTCH target genes, thereby establishing a role for KDM5A in SCLC tumorigenesis.