Abstract:
:Prolonged cell survival occurs through the expression of specific protein isoforms generated by alternate splicing of mRNA precursors in cancer cells. How alternate splicing regulates tumor development and resistance to targeted therapies in cancer remain poorly understood. Here we show that RNF113A, whose loss-of-function causes the X-linked trichothiodystrophy, is overexpressed in lung cancer and protects from Cisplatin-dependent cell death. RNF113A is a RNA-binding protein which regulates the splicing of multiple candidates involved in cell survival. RNF113A deficiency triggers cell death upon DNA damage through multiple mechanisms, including apoptosis via the destabilization of the prosurvival protein MCL-1, ferroptosis due to enhanced SAT1 expression, and increased production of ROS due to altered Noxa1 expression. RNF113A deficiency circumvents the resistance to Cisplatin and to BCL-2 inhibitors through the destabilization of MCL-1, which thus defines spliceosome inhibitors as a therapeutic approach to treat tumors showing acquired resistance to specific drugs due to MCL-1 stabilization.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Shostak K,Jiang Z,Charloteaux B,Mayer A,Habraken Y,Tharun L,Klein S,Xu X,Duong HQ,Vislovukh A,Close P,Florin A,Rambow F,Marine JC,Büttner R,Chariot Adoi
10.1038/s41467-020-15003-7subject
Has Abstractpub_date
2020-03-09 00:00:00pages
1270issue
1issn
2041-1723pii
10.1038/s41467-020-15003-7journal_volume
11pub_type
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