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Effect of RBN-2397, paclitaxel and their combination on ovarian cancer cell biology.

ABSTRACT: Effect of RBN-2397, paclitaxel and their combination on ovarian cancer cell biology.

PROVIDER: PRJNA1119560 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29269845.fastq.gz	Fastqsanger.gz
	SRR29269846.fastq.gz	Fastqsanger.gz
	SRR29269847.fastq.gz	Fastqsanger.gz
	SRR29269848.fastq.gz	Fastqsanger.gz
	SRR29269849.fastq.gz	Fastqsanger.gz

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Effect of RBN-2397, paclitaxel and their combination on ovarian cancer cell biology.

Project description:PARP7 (TiPARP), a mono (ADP-ribosyl) transferase (MART) was found to target α-tubulin proteins in ovarian cancer cells, enhancing their growth and migration. RBN-2397 is a potent inhibitor that selectively acts on PARP7. Here, we show that RBN-2397 treatment leads to the stabilization of microtubules in ovarian cancer cells, namely α-tubulin, mimicking what was previously observed with PARP7 knockdown. When treated with RBN-2397, we observe a decrease in growth and migration of ovarian cancer cells and, interestingly, the effect is intensified upon adding the microtubule stabilizing chemotherapeutic agent, paclitaxel. Mutating the site of α-tubulin MARylation by PARP7 similarly results in α-tubulin stabilization and decreased cell migration in the presence of paclitaxel when the tubulin network is further stabilized. In sum, we demonstrate that PARP7 inhibition decreases α-tubulin MARylation resulting in its stabilization, and ultimately leading to decreased ovarian cancer cell proliferation and migration. Finally, we show that combining PARP7 inhibitor and paclitaxel results in a more robust inhibition of aggressive ovarian cancer phenotypes. Collectively, this study highlights the potential of targeting PARP7 in combination with established chemotherapeutic agents to enhance treatment efficacy for ovarian cancer.

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Gene expression associated with acquired paclitaxel resistance in ovarian cancer cell lines

Project description:Conventional frontline treatment for ovarian cancer consists of successive chemotherapy cycles of paclitaxel and platinum. Despite the initial favorable responses for most patients, chemotherapy resistance frequently leads to recurrent or refractory disease. New treatment strategies that circumvent or prevent mechanisms of resistance are needed to improve ovarian cancer therapy. We developed in vitro ovarian cancer cell line models of acquired paclitaxel resistance using 2 immortalized human ovarian cancer cell lines, OVCAR3 and TOV-21G. We also developed in vitro primary ovarian cancer organoid models using tumor tissue from 7 patients with gynecologic malignancies. Gene expression differences in resistant and sensitive lines were analyzed by RNA sequencing to identify potential mechanisms of paclitaxel resistance in primary ovarian cancer.

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Ovarian cancer cell lines treated with eribulin and paclitaxel

Project description:Eribulin mesylate is a synthetic macrocyclic ketone analog of the marine sponge natural product halichondrin B. Eribulin is a mechanistically unique inhibitor of microtubule dynamics, leading to inhibition of microtubule growth in the absence of effects on microtubule shortening at microtubule plus ends, and formation of nonproductive tubulin aggregates. In this study, we investigated whether selective signal pathways were associated with eribulin activity compared to paclitaxel, which stabilizes microtubules, based on gene expression profiling of cell line panels of breast, endometrial, and ovarian cancer in vitro. 21 ovarian cancer cell lines treated with eribulin and paclitaxel for 24 hours at concentration 10xIC50. Three technical replicates were included for eribulin , paclitaxel and untreated cell lines.

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Paclitaxel resistance in ovarian cancer increases oncolytic adenovirus efficacy via upregulated CAR expression and dysfunctional cell cycle control

Project description:The microtubule-stabilising drug paclitaxel has activity in relapsed ovarian cancer. However, resistance frequently develops. Oncolytic adenoviruses are a novel cancer therapy, and replicate selectively within and lyse malignant cells, leading to productive infection of neighbouring cells. We found increased efficacy of adenoviruses of multiple subtypes in paclitaxel-resistant ovarian cancer cells. There was increased expression of a key adenovirus receptor, CAR (coxsackie adenovirus receptor), due to increased transcription that resulted from histone modification. Moreover, CAR transcription increased in intraperitoneal xenografts with acquired paclitaxel resistance and in tumours from patients with paclitaxel-resistant ovarian cancer. Finally, we identified dysregulated cell cycle control as a second mechanism of increased adenovirus efficacy in paclitaxel-resistant ovarian cancer and that inhibition of CDK4/6 using PD-0332991 was able both to reverse paclitaxel resistance and reduce adenovirus efficacy. Thus, paclitaxel resistance increases oncolytic adenovirus efficacy via at least two separate mechanisms. Parental SKOV3 and paclitaxel-resistant SKOV3-TR cells were analysed in duplicate

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Paclitaxel resistance in ovarian cancer increases oncolytic adenovirus efficacy via upregulated CAR expression and dysfunctional cell cycle control

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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.

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Ovarian cancer cell lines treated with eribulin and paclitaxel

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Hs 294T Cells Treated with Elesclomol Alone or in Combination with Paclitaxel Compared to DMSO Treated

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