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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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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

Breast cancer cell lines treated with eribulin and paclitaxel

2014-10-02 | GSE50811 | GEO

Endometrial cancer cell lines treated with eribulin and paclitaxel

2014-10-02 | GSE50830 | 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

Transcription Level Response of HEK-293T Cells to RfA1 Expression

Project description:We transfected HEK-293T cells to express RfA1. The RNA-Seq results indicates that Genes evolved in biological processes such as “regulation of microtubule cytoskeleton organization”, “microtubule polymerization or depolymerization”, “microtubule nucleation” were found to respond to RfA1 expression. Correspondingly, these microtubule relevant genes were also sorted to cellular component items, including “spindle microtubule”, “spindle pole centrosome”, “mitotic spindle”, “spindle” , which indicates the tight relationship between RfA1 and microtubules.

2021-11-01 | GSE186861 | GEO

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