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

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

PROVIDER: PRJNA644339 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12151572_1.fastq.gz	Fastqsanger.gz
	SRR12151572_2.fastq.gz	Fastqsanger.gz
	SRR12151573_1.fastq.gz	Fastqsanger.gz
	SRR12151573_2.fastq.gz	Fastqsanger.gz
	SRR12151574_1.fastq.gz	Fastqsanger.gz

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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.

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Project description:RNA-sequencing was performed to gain insight into the mechanism responsible for the mesenchymal-to-epithelial transition (MET) induced by loss of long non-coding RNA (lncRNA) DNM3OS in SKOV3 ovarian cancer cells. Following siRNA-mediated knockdown of DNM3OS or non-targeting control, RNA-sequencing was performed. This high-throughput data revealed knockdown of DNM3OS down-regulated the expression of genes and pathways known to induce EMT in ovarian cancer.

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