Abstract：
:The promyelocytic leukemia (PML) protein is an essential component of PML nuclear bodies (PML NBs) frequently lost in cancer. PML NBs coordinate chromosomal regions via modification of nuclear proteins that in turn may regulate genes in the vicinity of these bodies. However, few PML NB-associated genes have been identified. PML and PML NBs can also regulate mTOR and cell fate decisions in response to cellular stresses. We now demonstrate that PML depletion in U2OS cells or TERT-immortalized normal human diploid fibroblasts results in decreased expression of the mTOR inhibitor DDIT4 (REDD1). DNA and RNA immuno-FISH reveal that PML NBs are closely associated with actively transcribed DDIT4 loci, implicating these bodies in regulation of basal DDIT4 expression. Although PML silencing did reduce the sensitivity of U2OS cells to metabolic stress induced by metformin, PML loss did not inhibit the upregulation of DDIT4 in response to metformin, hypoxia-like (CoCl2) or genotoxic stress. Analysis of publicly available cancer data also revealed a significant correlation between PML and DDIT4 expression in several cancer types (e.g. lung, breast, prostate). Thus, these findings uncover a novel mechanism by which PML loss may contribute to mTOR activation and cancer progression via dysregulation of basal DDIT4 gene expression.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Salsman J,Stathakis A,Parker E,Chung D,Anthes LE,Koskowich KL,Lahsaee S,Gaston D,Kukurba KR,Smith KS,Chute IC,Léger D,Frost LD,Montgomery SB,Lewis SM,Eskiw C,Dellaire Gdoi
10.1038/srep45038subject
Has Abstractpub_date
2017-03-23 00:00:00pages
45038issn
2045-2322pii
srep45038journal_volume
7pub_type
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