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The splicing factor DHX38/PRP16 is required for ovarian clear cell carcinoma tumorigenesis, as revealed by a CRISPR-Cas9 screen

ABSTRACT: The splicing factor DHX38/PRP16 is required for ovarian clear cell carcinoma tumorigenesis, as revealed by a CRISPR-Cas9 screen

PROVIDER: PRJNA779052 | ENA |

REPOSITORIES: ENA

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The splicing factor DHX38/PRP16 is required for ovarian clear cell carcinoma tumorigenesis, as revealed by a CRISPR-Cas9 screen

Project description:Certain cancers, such as ovarian clear cell carcinoma (OCCC), display high levels of genetic variation between patients, confounding the development of effective therapies. In order to identify novel genes critical to OCCC growth, we employed the pooled genome-scale CRISPR Knock-Out (GeCKO) v2 CRISPR-Cas9 knockout screening system using the OCCC cell line JHOC5, as well as the T-antigen immortalized normal ovarian surface epithelium cell line OSE3 as a negative control. We identified the gene encoding DHX38/PRP16, an ATP-dependent RNA helicase involved in splicing, as critical for the growth and tumorigenesis of OCCC; DHX38 knockdown in OCCC cells, but not normal cells, induces apoptosis and impairs OCCC tumorigenesis in a mouse model. Our results suggest that DHX38/PRP16 may play a role in OCCC tumorigenesis, and can be regarded as a promising therapeutic target.

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Metabolic resistance to the inhibition of mitochondrial transcription revealed by CRISPR-Cas9 screen

Project description:Cancer cells depend on mitochondria to sustain their increased metabolic needs therefore, mitochondria constitute an interesting target for cancer treatment. We recently developed novel small-molecule inhibitors of mitochondrial transcription (IMTs) that selectively target mitochondrial gene expression. IMTs showed potent antitumor properties in vitro and in vivo, without affecting normal tissues. Because therapy-induced resistance is a major constraint to successful cancer therapy, we investigated mechanisms involved in resistance to IMTs. We employed a CRISPR-Cas9 whole genome screen to determine pathways responsible for resistance to acute IMT1 treatment. Loss of genes belonging to VHL and mTORC1 pathways caused IMT1 resistance. The relevance of these pathways was then validated by chemical modulation of these processes in cancer cells. We also generated IMT1-resistant cells to dissect responses to chronic mitochondrial gene expression impairment. We report that acquired resistance to IMT1 occurs through compensatory increase of mtDNA levels, transcripts and proteins. We found that chloramphenicol-mediated inhibition of mitochondrial translation impaired resistant cells’ survival. The identified susceptibility and resistance mechanisms to IMTs are important for future pharmacological interventions with mitochondria-targeted therapies.

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