CRISPR activation screens identify the SWI/SNF ATPases as suppressors of ferroptosis Article Swipe
Kamakoti P. Bhat
,
Jinchu Vijay
,
Caroline K. Vilas
,
Jyoti Asundi
,
Jun Zou
,
Ted Lau
,
Xiaoyu Cai
,
Musaddeque Ahmed
,
Michał Kabza
,
Julie Weng
,
Jean‐Philippe Fortin
,
Aaron T. L. Lun
,
Steffen Durinck
,
Marc Hafner
,
Michael R. Costa
,
Xin Ye
·
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1016/j.celrep.2024.114345
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1016/j.celrep.2024.114345
Ferroptosis is an iron-dependent cell death mechanism characterized by the accumulation of toxic lipid peroxides and cell membrane rupture. GPX4 (glutathione peroxidase 4) prevents ferroptosis by reducing these lipid peroxides into lipid alcohols. Ferroptosis induction by GPX4 inhibition has emerged as a vulnerability of cancer cells, highlighting the need to identify ferroptosis regulators that may be exploited therapeutically. Through genome-wide CRISPR activation screens, we identify the SWI/SNF (switch/sucrose non-fermentable) ATPases BRM (SMARCA2) and BRG1 (SMARCA4) as ferroptosis suppressors. Mechanistically, they bind to and increase chromatin accessibility at NRF2 target loci, thus boosting NRF2 transcriptional output to counter lipid peroxidation and confer resistance to GPX4 inhibition. We further demonstrate that the BRM/BRG1 ferroptosis connection can be leveraged to enhance the paralog dependency of BRG1 mutant cancer cells on BRM. Our data reveal ferroptosis induction as a potential avenue for broadening the efficacy of BRM degraders/inhibitors and define a specific genetic context for exploiting GPX4 dependency.
Related Topics
Concepts
GPX4
Cell biology
Chemistry
CRISPR
Biology
Programmed cell death
Genetics
Gene
Biochemistry
Glutathione
Glutathione peroxidase
Enzyme
Apoptosis
Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1016/j.celrep.2024.114345
- http://www.cell.com/article/S2211124724006739/pdf
- OA Status
- gold
- Cited By
- 11
- References
- 90
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4399588637
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4399588637Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1016/j.celrep.2024.114345Digital Object Identifier
- Title
-
CRISPR activation screens identify the SWI/SNF ATPases as suppressors of ferroptosisWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2024Year of publication
- Publication date
-
2024-06-01Full publication date if available
- Authors
-
Kamakoti P. Bhat, Jinchu Vijay, Caroline K. Vilas, Jyoti Asundi, Jun Zou, Ted Lau, Xiaoyu Cai, Musaddeque Ahmed, Michał Kabza, Julie Weng, Jean‐Philippe Fortin, Aaron T. L. Lun, Steffen Durinck, Marc Hafner, Michael R. Costa, Xin YeList of authors in order
- Landing page
-
https://doi.org/10.1016/j.celrep.2024.114345Publisher landing page
- PDF URL
-
https://www.cell.com/article/S2211124724006739/pdfDirect link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
-
https://www.cell.com/article/S2211124724006739/pdfDirect OA link when available
- Concepts
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GPX4, Cell biology, Chemistry, CRISPR, Biology, Programmed cell death, Genetics, Gene, Biochemistry, Glutathione, Glutathione peroxidase, Enzyme, ApoptosisTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
11Total citation count in OpenAlex
- Citations by year (recent)
-
2025: 10, 2024: 1Per-year citation counts (last 5 years)
- References (count)
-
90Number of works referenced by this work
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.CRISPR | 60 |
| abstract_inverted_index.avenue | 136 |
| abstract_inverted_index.cancer | 44, 124 |
| abstract_inverted_index.cells, | 45 |
| abstract_inverted_index.confer | 100 |
| abstract_inverted_index.define | 145 |
| abstract_inverted_index.mutant | 123 |
| abstract_inverted_index.output | 94 |
| abstract_inverted_index.reveal | 130 |
| abstract_inverted_index.target | 88 |
| abstract_inverted_index.ATPases | 69 |
| abstract_inverted_index.SWI/SNF | 66 |
| abstract_inverted_index.Through | 58 |
| abstract_inverted_index.context | 149 |
| abstract_inverted_index.counter | 96 |
| abstract_inverted_index.emerged | 39 |
| abstract_inverted_index.enhance | 117 |
| abstract_inverted_index.further | 106 |
| abstract_inverted_index.genetic | 148 |
| abstract_inverted_index.paralog | 119 |
| abstract_inverted_index.BRM/BRG1 | 110 |
| abstract_inverted_index.boosting | 91 |
| abstract_inverted_index.efficacy | 140 |
| abstract_inverted_index.identify | 50, 64 |
| abstract_inverted_index.increase | 83 |
| abstract_inverted_index.membrane | 17 |
| abstract_inverted_index.prevents | 23 |
| abstract_inverted_index.reducing | 26 |
| abstract_inverted_index.rupture. | 18 |
| abstract_inverted_index.screens, | 62 |
| abstract_inverted_index.specific | 147 |
| abstract_inverted_index.(SMARCA2) | 71 |
| abstract_inverted_index.(SMARCA4) | 74 |
| abstract_inverted_index.alcohols. | 32 |
| abstract_inverted_index.chromatin | 84 |
| abstract_inverted_index.exploited | 56 |
| abstract_inverted_index.induction | 34, 132 |
| abstract_inverted_index.leveraged | 115 |
| abstract_inverted_index.mechanism | 6 |
| abstract_inverted_index.peroxides | 14, 29 |
| abstract_inverted_index.potential | 135 |
| abstract_inverted_index.activation | 61 |
| abstract_inverted_index.broadening | 138 |
| abstract_inverted_index.connection | 112 |
| abstract_inverted_index.dependency | 120 |
| abstract_inverted_index.exploiting | 151 |
| abstract_inverted_index.inhibition | 37 |
| abstract_inverted_index.peroxidase | 21 |
| abstract_inverted_index.regulators | 52 |
| abstract_inverted_index.resistance | 101 |
| abstract_inverted_index.Ferroptosis | 0, 33 |
| abstract_inverted_index.demonstrate | 107 |
| abstract_inverted_index.dependency. | 153 |
| abstract_inverted_index.ferroptosis | 24, 51, 76, 111, 131 |
| abstract_inverted_index.genome-wide | 59 |
| abstract_inverted_index.inhibition. | 104 |
| abstract_inverted_index.(glutathione | 20 |
| abstract_inverted_index.accumulation | 10 |
| abstract_inverted_index.highlighting | 46 |
| abstract_inverted_index.peroxidation | 98 |
| abstract_inverted_index.suppressors. | 77 |
| abstract_inverted_index.accessibility | 85 |
| abstract_inverted_index.characterized | 7 |
| abstract_inverted_index.vulnerability | 42 |
| abstract_inverted_index.iron-dependent | 3 |
| abstract_inverted_index.(switch/sucrose | 67 |
| abstract_inverted_index.transcriptional | 93 |
| abstract_inverted_index.Mechanistically, | 78 |
| abstract_inverted_index.non-fermentable) | 68 |
| abstract_inverted_index.therapeutically. | 57 |
| abstract_inverted_index.degraders/inhibitors | 143 |
| cited_by_percentile_year.max | 99 |
| cited_by_percentile_year.min | 90 |
| corresponding_author_ids | https://openalex.org/A5100348104 |
| countries_distinct_count | 2 |
| institutions_distinct_count | 16 |
| citation_normalized_percentile.value | 0.93261929 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | True |