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| Status |
Public on Sep 16, 2020 |
| Title |
Plasticity of ether lipids promotes ferroptosis susceptibility and evasion |
| Organism |
Homo sapiens |
| Experiment type |
Other
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| Summary |
Ferroptosis, an iron-dependent, non-apoptotic cell death program, is involved in a variety of degenerative diseases and represents a targetable vulnerability in certain cancers. The ferroptosis-susceptible cell-state can either preexist in cells arising from certain lineages or be acquired during cell-state transitions. Precisely how ferroptosis susceptibility is dynamically regulated remains poorly understood. Using genome-wide CRISPR/Cas9 suppressor screens, we identify a key role for peroxisome–ether phospholipid genes in driving ferroptosis susceptibility and evasion in ovarian cancer.
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| Overall design |
Ovcar8 CRISPR library infected cells treated with escalating doses of RSL3 (Selleckchem) for 4 days each: 0.5 μM, 1 μM, and 2μM. 1×10^7 cells each were collected from the surviving population of RSL3-treated cells and an endpoint-matched untreated population for downstream sequencing analysis.
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| Contributor(s) |
Henry WS, Keys HR |
| Citation missing |
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| |
| Submission date |
May 22, 2020 |
| Last update date |
Sep 18, 2020 |
| Contact name |
Yilong Zou |
| E-mail(s) |
yzou@broadinstitute.org
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| Organization name |
Broad Institute of MIT and Harvard
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| Department |
Chemical Biology and Therapeutic Sciences
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| Street address |
415 Main Street
|
| City |
Cambridge |
| State/province |
MASSACHUSETTS |
| ZIP/Postal code |
02142 |
| Country |
USA |
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| Platforms (1) |
| GPL16791 |
Illumina HiSeq 2500 (Homo sapiens) |
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| Samples (6)
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| Relations |
| BioProject |
PRJNA634531 |
| SRA |
SRP262968 |
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