Abstract:
:Ferroptosis is a newly discovered form of non-apoptotic cell death in multiple human diseases. However, the epigenetic mechanisms underlying ferroptosis remain poorly defined. First, we demonstrated that lymphoid-specific helicase (LSH), which is a DNA methylation modifier, interacted with WDR76 to inhibit ferroptosis by activating lipid metabolism-associated genes, including GLUT1, and ferroptosis related genes SCD1 and FADS2, in turn, involved in the Warburg effect. WDR76 targeted these genes expression in dependent manner of LSH and chromatin modification in DNA methylation and histone modification. These effects were dependent on iron and lipid reactive oxygen species. We further demonstrated that EGLN1 and c-Myc directly activated the expression of LSH by inhibiting HIF-1α. Finally, we demonstrated that LSH functioned as an oncogene in lung cancer in vitro and in vivo. Therefore, our study elucidates the molecular basis of the c-Myc/EGLN1-mediated induction of LSH expression that inhibits ferroptosis, which can be exploited for the development of therapeutic strategies targeting ferroptosis for the treatment of cancer.
journal_name
Theranosticsjournal_title
Theranosticsauthors
Jiang Y,Mao C,Yang R,Yan B,Shi Y,Liu X,Lai W,Liu Y,Wang X,Xiao D,Zhou H,Cheng Y,Yu F,Cao Y,Liu S,Yan Q,Tao Ydoi
10.7150/thno.19988subject
Has Abstractpub_date
2017-07-23 00:00:00pages
3293-3305issue
13issn
1838-7640pii
thnov07p3293journal_volume
7pub_type
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