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RNA Sequencing of 16D Prostate Cancer Cell Lines with genetic knockout of OGDHL

ABSTRACT: The goal of this study was to perform transcriptomics of prostate cancer cells with genetic knockout of OGDHL treated with the Androgen Receptor Pathway Inhibitor Enzalutamide (Enza) or Vehicle (DMSO)

ORGANISM(S): Homo sapiens

PROVIDER: GSE298123 | GEO | 2025/06/06

REPOSITORIES: GEO

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Identification of Radiosensitivity Gene Signatures Induced by Enzalutamide in Prostate cancer cells

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Chromatin Occupancy of AR, BRD4, and H3K27Ac in MR42D Cells in response to Enzalutamide [RNA-seq]

Project description:To identify mechanisms that contribute to lineage plasticity and t-NEPC, we focused on enza-resistant cell lines with persistent AR expression that have features of lineage plasticity, including high expression of NEPC markers: the MR42D and MR42F cell lines. We cultured these enzalutamide resistant lines, which are usually maintained in medium with enzalutamide, without enzalutamide for 72 hors to "washout" the effects of enzalutamide, and then either enzalutamide or vehicle was added back to the growing media for 24 hours. Enzalutamide sensitive lines LNCaP and V16D were treated with either enzalutamide or vehicle for 24 hours. Enzalutamide reversibly increased expression neuronal markers in MR42D and MR42F cells, but not enza-sentitive LNCaP and V16D cells, suggesting that the AR may negatively regulate neuronal gene expression in these t-NEPC cells. Moreover, bromodomain inhibitors (BETi) ARV-771 and JQ1 reduced expression of NEPC target genes in MR42D cells.

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RNA-seq analysis regarding antiandrogen (enzalutamide) effect on gene expression in castration-resistant prostate cancer (CRPC) xenograft model

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