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RNA sequencing of HJURP silencing in ovarian cancer cells

ABSTRACT: RNA sequencing of HJURP silencing in ovarian cancer cells

PROVIDER: PRJNA787567 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17182344_1.fastq.gz	Fastqsanger.gz
	SRR17182344_2.fastq.gz	Fastqsanger.gz
	SRR17182345_1.fastq.gz	Fastqsanger.gz
	SRR17182345_2.fastq.gz	Fastqsanger.gz
	SRR17182346_1.fastq.gz	Fastqsanger.gz

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RNA sequencing of HJURP silencing in ovarian cancer cells

Project description:Ovarian cancer is the most lethal gynecological malignancy. Recurrence and chemoresistance are tough challenges leading to poor prognosis. HJURP is a molecular chaperone of CENP-A, which is associated with aggressive progression in multiple tumors. However, the function of HJURP in ovarian cancer has not been elucidated. In our study, we found HJURP was over-expressed in ovarian cancer and high expression of HJURP was correlated to unfavorable prognosis. HJURP knockdown could inhibit proliferation, metastasis and induce G0/G1 stagnation of ovarian cancer cells. Besides, next-generation sequencing(NGS) unveiled that WEE1 was down-regulated by silencing HJURP. Further mechanistic research revealed that HJURP regulated WEE1 through MYC, and luciferase assay indicated that MYC was a transcription factor of WEE1. Additionally, we investigated that silencing HJURP increased sensitivity of ovarian cancer cells to cisplatin via MYC/WEE1 axis, and HJURP participated in DNA repair of cisplatin-induced damage. More interestingly, silencing HJURP could enhance sensitivity of ovarian cancer cells to AZD1775 and improve the synergistic effect of cisplatin plus AZD1775 combined therapy. Collectively, our data displays that HJURP promotes tumor progression and chemoresistance of ovarian cancer, and HJURP has potential to be a novel therapeutic target in the combined treatment with cisplatin and AZD1775 in ovarian cancer.

2022-01-26 | GSE190568 | GEO

Transcriptional profile of CAOV2 ovarian cancer cells with YAP silencing

Project description:Transcriptional profile of CAOV2 ovarian cancer cells with YAP silencing

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Transcriptional profile of CAOV2 ovarian cancer cells with YAP silencing

Project description:We performed RNAseq to study the transcriptional changes of human CAOV2 ovarian cancer cells with or without YAP silencing by siRNAs to understand the genetic determinants of ferroptosis response

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Transcriptional profile of CAOV2 ovarian cancer cells with TAZ silencing

Project description:We performed RNAseq to study the transcriptional changes of human CAOV2 ovarian cancer cells with or without TAZ silencing by siRNAs to understand the genetic determinants of ferroptosis response

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Comparisons of the global gene profile between CLDN4-overexpressing and CLDN4-silencing ovarian cancer cells.

Project description:A microarray analysis was performed to compare the global gene expression profile between CLDN4-overexpressing (Control) and CLDN4-silencing SKOV-3 ovarian cancer cells. CLDN4 gene was knocked down by CLDN4 siRNA lentivirus. Total RNA was extracted and microarray was perfomed to compare the gene profiling changes between CLDN4-overexpressing (Control) and CLDN4-silencing cells. The experiment was performed in triplicate.

2010-12-15 | E-GEOD-22493 | biostudies-arrayexpress

RNA sequencing of ovarian cancer cells treated by Paeonol

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Comparisons of the global gene profile between CLDN4-overexpressing and CLDN4-silencing ovarian cancer cells.

Project description:A microarray analysis was performed to compare the global gene expression profile between CLDN4-overexpressing (Control) and CLDN4-silencing SKOV-3 ovarian cancer cells.

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RNA sequencing (RNA-seq) of PQBP1 knockdown in ovarian cancer cells

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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

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