Genome-wide CRISPR screening identifies a role for ARRDC3 in TRP53-mediated responses

La Marca, JE; Aubrey, BJ; Yang, B; Chang, C; Wang, Z; Kueh, A; Tai, L; Wilcox, S; Milla, L; Heinzel, S; Vremec, D; Whelan, L; K&#246;nig, C; Kaloni, D; Voss, AK; Strasser, A; Diepstraten, ST; Herold, MJ; Kelly, GL

Author(s): La Marca, JE; Aubrey, BJ; Yang, B; Chang, C; Wang, Z; Kueh, A; Tai, L; Wilcox, S; Milla, L; Heinzel, S; Vremec, D; Whelan, L; König, C; Kaloni, D; Voss, AK; Strasser, A; Diepstraten, ST; Herold, MJ; Kelly, GL;
Details: Publication Year 2024-12-14,Volume 31,Issue #2,Page 150-158
Journal Title: Cell Death and Differentiation
Abstract: 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.
Publisher: Springer Nature
Keywords: Animals; Mice; Arrestins/genetics/metabolism; Clustered Regularly Interspaced Short Palindromic Repeats; *Lymphoma; *Neoplasms/genetics
Research Division(s): Advanced Technology And Biology; Epigenetics And Development; Immunology; Blood Cells And Blood Cancer; Advanced Technology and Biology; Immunology; Epigenetics and Development
PubMed ID: 38097622
Publisher's Version: https://doi.org/10.1038/s41418-023-01249-3
Open Access at Publisher's Site: https://doi.org/10.1038/s41418-023-01249-
Terms of Use/Rights Notice: Refer to copyright notice on published article.

Creation Date: 2023-12-21 07:38:40

Last Modified: 2024-03-05 09:29:06