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Ovarian cancer cell lines treated with eribulin and paclitaxel

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Zoltan Dezso

PROVIDER: E-GEOD-50831 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Breast 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. 27 breast 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.

2014-10-02 | E-GEOD-50811 | biostudies-arrayexpress

Endometrial 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. 19 endometrial 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.

2014-10-02 | E-GEOD-50830 | biostudies-arrayexpress

Ovarian cancer cell lines treated with eribulin and paclitaxel

2014-10-02 | GSE50831 | GEO

Endometrial cancer cell lines treated with eribulin and paclitaxel

2014-10-02 | GSE50830 | GEO

Breast cancer cell lines treated with eribulin and paclitaxel

2014-10-02 | GSE50811 | GEO

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.

2024-10-01 | GSE268985 | GEO

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

2015-12-10 | E-GEOD-54772 | biostudies-arrayexpress

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

2015-12-10 | GSE54772 | GEO

Gene Expression Profiling Reveals Epithelial Mesenchymal Transition (EMT) Genes Can Selectively Differentiate Eribulin Sensitive Breast Cancer Cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-10-02 | E-GEOD-50832 | biostudies-arrayexpress

Phosphoproteomic analysis of neoadjuvant breast cancer reveals a subset of patients with increased sensitivity to paclitaxel driven by CDK4 and Filamin A.

Project description:Precision oncology research is challenging outside contexts of oncogenic addiction and/or targeted therapies. We previously showed that phosphoproteomics is a powerful approach to reveal patient subsets of interest characterized by the activity of a few kinases where the underlying genomics is complex. Here, we conducted a phosphoproteomic screening in a neoadjuvant trial of HER2-negative breast cancer patients (N=130) treated with paclitaxel or paclitaxel plus nintedanib, aiming to find candidate biomarkers of paclitaxel sensitivity. Filtering 15 candidate biomarkers through 2 independent patient sets (N=218) allowed finding a subgroup of patients characterized by high levels of CDK4 and Filamin-A, who had a 90% chance of achieving a pCR in response to paclitaxel. Mechanistically, CDK4 regulated Filamin-A transcription, which in turn formed a complex with Tubulin and CLIP-170, what elicited increased binding of paclitaxel to microtubules, microtubule acetylation and stabilization, and mitotic catastrophe. Thus, phosphoproteomics allowed finding explainable predictive factors for paclitaxel.

2022-11-08 | PXD034355 | Pride

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