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RNA sequencing of MEX3A knockdown by siRNA in ovarian cancer cells

ABSTRACT: RNA sequencing of MEX3A knockdown by siRNA in ovarian cancer cells

PROVIDER: PRJNA782974 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17017922_1.fastq.gz	Fastqsanger.gz
	SRR17017922_2.fastq.gz	Fastqsanger.gz
	SRR17017924_1.fastq.gz	Fastqsanger.gz
	SRR17017924_2.fastq.gz	Fastqsanger.gz
	SRR17017925_1.fastq.gz	Fastqsanger.gz

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RNA sequencing of MEX3A knockdown by siRNA in ovarian cancer cells

Project description:RNA-binding proteins can serve as novel potential targets for cancer therapy. We used bioinformatics analysis to screen and identify the key RBPs in ovarian cancer (OC), from which we found that Mex-3 RNA Binding Family Member A (MEX3A) was intimately associated with the clinical prognosis of OC. High expression of MEX3A was involved in the malignant proliferation and aggressiveness of ovarian cancer.

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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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RNA sequencing of SF3B4 knockdown by siRNA in ovarian cancer cells

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RNA sequencing (RNA-SEQ) of RECQL4 knockdown by siRNA in ovarian cancer cells

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RNA sequencing (RNA-SEQ) of FOXM1 knockdown by siRNA in ovarian cancer cells

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siRNA-mediated knockdown

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RNA sequencing (RNA-SEQ) of RECQL4 knockdown by siRNA in ovarian cancer cells

Project description:The high frequency of somatic copy number alterations, as opposed to point mutations, is considered a unique feature of high-grade serous ovarian carcinoma (HGSOC). Amplification-dependent overexpression of RECQL4, which participates in DNA replication and repair, mediates the development of various cancers, but its pathobiological and clinical roles are poorly understood. Here, using bioinformatics analysis, RECQL4 amplification was found to occur in 27% of HGSOC samples in the TCGA cohort. RECQL4 was found to be upregulated and associated with a poor prognosis based on the immunohistochemistry staining of HGSOC. Functionally, RECQL4 overexpression increased proliferation and invasion of ovarian cancer cells both in vitro and in vivo. RECQL4 silencing had the opposite effects. In addition, RECQL4 knockdown enhanced the sensitivity of ovarian cancer cells to cisplatin and PARP inhibitor (PARPi). Further mechanistic investigations revealed that MAFB was a downstream target of RECQL4. The oncogenic effect of RECQL4 was attenuated after MAFB knockdown. Moreover, RECQL4 overexpression was negatively regulated by the tumour suppressor miR-10a-5p. Collectively, these findings indicate that genomic amplification and low expression of miR-10a-5p contribute to RECQL4 overexpression in ovarian cancer. This is the first study to reveal the oncogenic functions and clinical significance of RECQL4 in ovarian cancer.

2020-10-13 | GSE153839 | GEO

Effects of FGFRL1 knockdown on gene expression in ovarian cancer cell lines

Project description:Analysis of ovarian cancer cell lines after knockdown of FGFRL1 using SiRNA. To elucidate the signaling pathways that were significantly altered following the silencing of FGFRL1 expression, we performed global gene profiling experiments of the OVCAR8 and ES2 cells after knockdown of FGFRL1 using siRNA. We conducted pathway analysis with the differentially expressed genes using R in two OC cells.

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