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H3K4me3 HiChIP for L3.6pl cells (parental and paclitaxel-resistant)

ABSTRACT: H3K4me3 HiChIP for L3.6pl cells (parental and paclitaxel-resistant)

PROVIDER: PRJEB52812 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR9723960_1.fastq.gz	Fastqsanger.gz
	ERR9723960_2.fastq.gz	Fastqsanger.gz
	ERR9723959_1.fastq.gz	Fastqsanger.gz
	ERR9723959_2.fastq.gz	Fastqsanger.gz

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H3K4me3 HiChIP for Paclitaxel resistant L3.6pl pancreatic cancer cells (Non targeting vs siJunD)

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leChRO-seq in L3.6pl (Parental and Paclitaxel-resistant)

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ATAC seq for L3.6pl cells: Parental and resistant to paclitaxel [PacR]

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H3K4me3 HiChIP for Paclitaxel resistant L3.6pl pancreatic cancer cells (Non targeting vs siJunD)

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H3K4me3 HiChIP for L3.6pl cells (parental and paclitaxel-resistant)

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4C-seq at iHUB regions in L3.6pl

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ChIP seq for H4K5ac, JunD , and MED1 in Parental and Paclitaxel resistant L3.6pl cell line

Project description:ChIP seq for H4K5ac, JunD , and MED1 in Parental and Paclitaxel resistant L3.6pl cell line

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ChIP seq for H3K27ac, BRD4, H3K4me3, Pol II and input in paclitaxel resistant L3.6pl cells ChIP for Pol II , H3K4me3 and input in parental L3.6pl

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Downregulation of miR-194-5p induces paclitaxel resistance in ovarian cancer cells by altering MDM2 expression.

Project description:Paclitaxel is a first-line drug for treating epithelial ovarian cancer (EOC). However, prognosis for patients with advanced stage cancer remains poor due to primary or acquired drug resistance. Therefore, overcoming chemoresistance is one of the greatest challenges in treating EOC. In this study, we identified microRNAs (miRNA) that regulate paclitaxel resistance and tested their potential utility as therapeutic targets. Paclitaxel-resistant cell lines were established using two EOC cell lines: SKVO3ip1 and HeyA8. miRNA PCR arrays showed that miR-194-5p was downregulated in paclitaxel-resistant cells. Forced expression of miR-194-5p resensitized resistant cells to paclitaxel. Conversely, miR-194-5p inhibition induced paclitaxel resistance in parental cells. In silico analysis and luciferase reporter assay revealed that MDM2 is a direct target of miR-194-5p. MDM2 was upregulated in paclitaxel resistant cells compared with parental cells. MDM2 inhibition also resensitized resistant cells to paclitaxel and forced MDM2 induced paclitaxel resistance in parental cells. miR-194-5p induced p21 upregulation and G1 phase arrest in resistant cells by downregulating MDM2. Furthermore, a public database showed that high MDM2 expression was associated with a shorter progression-free survival in EOC patients treated with paclitaxel. Collectively, our results show that restoring miR-194-5p expression resensitizes EOCs to paclitaxel, and this may be exploited as a therapeutic option.

2019-10-18 | GSE139043 | GEO

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