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Tubulin mRNA stability is sensitive to change in microtubule dynamics caused by multiple physiological and toxic cues

ABSTRACT: The goal of this study is to compare gene expression profiles in quiescent RPE1 hTert cells treated with microtubule-stabilizing (paclitaxel) and microtubule-destabilizing poisons (combretastatin A4)

ORGANISM(S): Homo sapiens

PROVIDER: GSE128414 | GEO | 2019/03/19

REPOSITORIES: GEO

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human hTERT-RPE1 cell spheroid : Control siRNA transfected vs. YAP1 siRNA transfected

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Gene expression in hTERT-RPE1 cells with overexpression of MFRP

Project description:Gene expression was compared between hTERT-RPE1 cells and hTERT-RPE1 cells stably overexpressing mouse MFRP with an N-terminal GFP fusion.

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Tubulin mRNA stability is sensitive to change in microtubule dynamics caused by multiple physiological and toxic cues

Project description:Tubulin mRNA stability is sensitive to change in microtubule dynamics caused by multiple physiological and toxic cues

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human hTERT-RPE1 cell spheroid : Control siRNA transfected vs. YAP1 siRNA transfected

Project description:Transcriptional profiling of human hTERT-RPE1 cell spheroids comparing Control siRNA transfected hTERT-RPE1 cell spheroids with those transfected with YAP1 siRNA. Two-condition experiment, Control siRNA vs.YAP1 siRNA hTERT-RPE1 cell spheroids. Biological replicates: 1 Control siRNA, 1YAP1 siRNA transfected, independently grown and harvested. Bothreplicates per array.

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Tubulin mRNA stability is sensitive to change in microtubule dynamics caused by multiple physiological and toxic cues.

Project description: Not available

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Project description:Gene expression was compared between hTERT-RPE1 cells and hTERT-RPE1 cells stably overexpressing mouse MFRP with an N-terminal GFP fusion. RNA was prepared from hTERT-RPE1 cells overexpressing GFP-MFRP and control cells. Both conditions were done in triplicate. Affymetrix GeneChip Human Genome U133Plus2.0 arrays were used to interrogate changes in gene expression. Image data were quantified with Affymetrix Expression Console Software and normalized with Robust Multichip Analysis.

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Project description:The lack of a cure for metastatic prostate cancer (PCa) highlights the urgent need for more efficient drugs to fight this disease. Here, we report the molecular mechanism of action of the natural product 6-acetoxy-anopterine (6-AA) in malignant cells of the prostate. This potent cytotoxic alkaloid from the endemic Australian tree Anopterus macleayanus induced at low nanomolar doses a strong accumulation of LNCaP and PC3 PCa cells in mitosis, severe mitotic spindle defects and asymmetric cell divisions, ultimately leading to mitotic catastrophe accompanied by cell death through apoptosis. DNA microarray of 6-AA treated LNCaP cells combined with pathway analysis identified very similar transcriptional changes when compared to vinblastine, highlighting pathways involved in mitosis, microtubule spindle organisation and microtubule binding. Like vinblastine, 6-AA inhibited microtubule polymerization in a cell-free system and reduced microtubule polymer mass in vitro. Yet, microtubule alterations that are associated with resistance to microtubule-destabilizing drugs like vinca alkaloids or 2-methoxyestradiol did not confer cross-resistance to 6-AA, suggesting a different mechanism of microtubule interaction. Finally, 6-AA is the first-in-class microtubule inhibitor that features the unique anopterine scaffold. Altogether, this study provides a strong rationale to further develop this novel structure class of microtubule inhibitor for the treatment of malignant disease.

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Stepwise chromatin loading of MCM hexamers toward onset of DNA replication

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