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ABSTRACT: wild-type loach and MEX3A gene knockout loach posterior intestine

PROVIDER: PRJNA1091403 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28433170_1.fastq.gz	Fastqsanger.gz
	SRR28433170_2.fastq.gz	Fastqsanger.gz
	SRR28433171_1.fastq.gz	Fastqsanger.gz
	SRR28433171_2.fastq.gz	Fastqsanger.gz
	SRR28433172_1.fastq.gz	Fastqsanger.gz

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MEX3A mediates p53 degradation to suppress ferroptosis and facilitate ovarian cancer tumorigenesis

Project description:Epithelial ovarian cancer (OC) is a highly heterogeneous and malignant female cancer with an overall low survival rate. p53 mutation is a predominant genetic factor thought to be responsible for poor clinical outcome. Despite the fact that ovarian clear cell carcinoma (OCCC) shows more severe prognosis, drug resistance, metastasis and recurrence compared to other OC subtypes, mutations in p53 are much less frequent. The underlying mechanisms crucial for tumorigenesis and malignancy of OC harboring wild-type (WT) p53 remain poorly understood. We found that upregulation of MEX3A, which is a dual-function protein containing a RING finger domain and an RNA binding domain, was correlated with poor survival in OC. MEX3A overexpression enhanced tumorigenic activity in RMG-1 and OVISE OCCC cell lines. In contrast, depletion of MEX3A in PA-1 ovarian teratocarcinoma cells and TOV21G OCCC cells reduced cell survival and proliferative ability in cell-based assays, as well as inhibited tumor growth and prolonged survival in orthotopic xenograft models. MEX3A depletion did not alter p53 mRNA level but did increase the protein stability of WT p53. MEX3A-mediated p53 protein degradation was crucial to prevent ferroptosis and enhance tumorigenesis as p53 knockdown reversed the effects of MEX3A depletion. Together, our observations identified MEX3A as an important oncogenic factor promoting tumorigenesis in OC cells harboring WT p53.

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