Genome-wide CRISPR screening identifies a role for ARRDC3 in TRP53-mediated responses
© 2023. The Author(s)..
Whole-genome screens using CRISPR technologies are powerful tools to identify novel tumour suppressors as well as factors that impact responses of malignant cells to anti-cancer agents. Applying this methodology to lymphoma cells, we conducted a genome-wide screen to identify novel inhibitors of tumour expansion that are induced by the tumour suppressor TRP53. We discovered that the absence of Arrestin domain containing 3 (ARRDC3) increases the survival and long-term competitiveness of MYC-driven lymphoma cells when treated with anti-cancer agents that activate TRP53. Deleting Arrdc3 in mice caused perinatal lethality due to various developmental abnormalities, including cardiac defects. Notably, the absence of ARRDC3 markedly accelerated MYC-driven lymphoma development. Thus, ARRDC3 is a new mediator of TRP53-mediated suppression of tumour expansion, and this discovery may open new avenues to harness this process for cancer therapy.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2024 |
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| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:31 |
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| Enthalten in: |
Cell death and differentiation - 31(2024), 2 vom: 21. Feb., Seite 150-158 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
La Marca, John E [VerfasserIn] |
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| Links: |
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| Themen: |
ARRDC3 protein, mouse |
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| Anmerkungen: |
Date Completed 12.02.2024 Date Revised 20.03.2024 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1038/s41418-023-01249-3 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| 520 | |a Whole-genome screens using CRISPR technologies are powerful tools to identify novel tumour suppressors as well as factors that impact responses of malignant cells to anti-cancer agents. Applying this methodology to lymphoma cells, we conducted a genome-wide screen to identify novel inhibitors of tumour expansion that are induced by the tumour suppressor TRP53. We discovered that the absence of Arrestin domain containing 3 (ARRDC3) increases the survival and long-term competitiveness of MYC-driven lymphoma cells when treated with anti-cancer agents that activate TRP53. Deleting Arrdc3 in mice caused perinatal lethality due to various developmental abnormalities, including cardiac defects. Notably, the absence of ARRDC3 markedly accelerated MYC-driven lymphoma development. Thus, ARRDC3 is a new mediator of TRP53-mediated suppression of tumour expansion, and this discovery may open new avenues to harness this process for cancer therapy | ||
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| 700 | 1 | |a Chang, Catherine |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Zilu |e verfasserin |4 aut | |
| 700 | 1 | |a Kueh, Andrew |e verfasserin |4 aut | |
| 700 | 1 | |a Tai, Lin |e verfasserin |4 aut | |
| 700 | 1 | |a Wilcox, Stephen |e verfasserin |4 aut | |
| 700 | 1 | |a Milla, Liz |e verfasserin |4 aut | |
| 700 | 1 | |a Heinzel, Susanne |e verfasserin |4 aut | |
| 700 | 1 | |a Vremec, David |e verfasserin |4 aut | |
| 700 | 1 | |a Whelan, Lauren |e verfasserin |4 aut | |
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| 700 | 1 | |a Diepstraten, Sarah T |e verfasserin |4 aut | |
| 700 | 1 | |a Herold, Marco J |e verfasserin |4 aut | |
| 700 | 1 | |a Kelly, Gemma L |e verfasserin |4 aut | |
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