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RNA-sequencing for the characterization of the transcriptome of SUM 159 parental and Paclitaxel (PTX) resistant breast cancer cells.

ABSTRACT: RNA-sequencing for the characterization of the transcriptome of SUM 159 parental and Paclitaxel (PTX) resistant breast cancer cells.

PROVIDER: PRJNA849791 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19668484.fastq.gz	Fastqsanger.gz
	SRR19668485.fastq.gz	Fastqsanger.gz
	SRR19668486.fastq.gz	Fastqsanger.gz
	SRR19668487.fastq.gz	Fastqsanger.gz
	SRR19668488.fastq.gz	Fastqsanger.gz

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RNA-sequencing for the characterization of the transcriptome of SUM 159 parental and Paclitaxel (PTX) resistant breast cancer cells.

Project description:RNA-sequencing was performed in SUM 159 parental and PTX resistant breast cancer cells in an effort to identify novel regulators of chemoresistance that could potentially be targeted in Triple Negative Breast Cancer (TNBC). The bioinformatic analysis identified numerous differentially expressed genes including several known chemoresistance markers, as well as novel genes that may play an important role in breast cancer chemoresistant cells.

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Gene Expression data from SH3GL2 overexpressing SUM-159 cells

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Paclitaxel resistant MDA-MB-231 Cells and resensitization with bexarotene treatment

Project description:Acquired drug resistance represents a major challenge in chemo-therapy treatment for various types of cancers. We have found that the retinoid X receptorâselective agonist bexarotene (LGD1069, Targretin) was efficacious in treating chemo-resistant cancer cells. The goal of this microarray study was to understand the mechanism of bexaroteneâs role in overcoming acquired drug resistance using human breast cancer cells MDA-MB-231 as a model system and paclitaxel as model compound. After MDA-MB-231 cells were repeatedly treated with paclitaxel for 8 cycles with each cycle including a 3-day treatment with 30 nM paclitaxel and followed by a 7-day exposure to control medium, MDA cells resistant to paclitaxel were developed and their growth was no longer inhibited by paclitaxel treatment. Those MDA cells with acquired drug resistance, when treated with paclitaxel and bexarotene in combination, could regain their sensitivity and their growth were again inhibited. Therefore, RNA samples from parental MDA-MB-231 cells, paclitaxel-resistant MDA cells treated with vehicle, paclitaxel alone or in combination with bexarotene, were used for perform global gene expression profiling with Affymetrix HG-U133A gene chips. Keywords: Drug Treatment MDA-MB-231 cells were exposed to regimens on a 10-day cycle: a 3-day treatment with 30 nM paclitaxel and followed by a 7-day exposure to control medium. Paclitaxel resistant MDA-MB-231 cells (MDA-PR) were established within 8 cycles of such treatment (80 days). These MDA-PR cells were then treated with vehicle control, paclitaxel along, or the combination of 30 nM paclitaxel ( 3 days on and 7 days off) and 1 ÂµM Targretin (10 days on) in a new 10-day cycle for 3 months. Thus, there are four treatment groups, parent MDA cells, MDA-PR, MDA-PR treated with paclitaxel, MDA-PR treated with paclitaxel and bexarotene, and each group had four biological replicates.

2011-07-18 | E-GEOD-12791 | biostudies-arrayexpress

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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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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