| First Author | La Marca JE | Year | 2024 |
| Journal | Cell Death Differ | Volume | 31 |
| Issue | 2 | Pages | 150-158 |
| PubMed ID | 38097622 | Mgi Jnum | J:345061 |
| Mgi Id | MGI:7581796 | Doi | 10.1038/s41418-023-01249-3 |
| Citation | La Marca JE, et al. (2024) Genome-wide CRISPR screening identifies a role for ARRDC3 in TRP53-mediated responses. Cell Death Differ 31(2):150-158 |
| abstractText | 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. |
