MiRNA expression profiles of MDA-MB-231 TNBC cells with defected RARalpha serine-77 phosphorylation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA672909 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12922277.fastq.gz | Fastqsanger.gz | |||
| SRR12922278.fastq.gz | Fastqsanger.gz | |||
| SRR12922279.fastq.gz | Fastqsanger.gz | |||
| SRR12922280.fastq.gz | Fastqsanger.gz | |||
| SRR12922281.fastq.gz | Fastqsanger.gz |
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Project description:microRNAs have been shown to be involved in the pathogenesis of TNBC as important regulators of cell proliferation and apoptosis. However, whether the activation of retinoic acid receptor alpha (RARα), a transcription factor, is involved in mediating transcriptional regulation of microRNAs remains elusive. Here, we investigated the differentially expressed miRNAs in triple negative breast cancer cell line MDA-MB-231 overexpressing a phosphorylation-defective mutant RARαS77A, which mimicked activated RARα, in comparison to non-transfected control cells.
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Project description:Triple-negative breast cancer (TNBC) is aggressive and difficult, and few targeted therapies are available to treat this patient population. The androgen receptor (AR) has emerged as a potential target in breast cancer. Newer generation AR inhibitors, such as Seviteronel (Sevi), are unique in their ability to inhibit AR both directly and by blocking upstream androgen synthesis. The purpose of this study was to investigate the pre-clinical activity of Sevi in TNBC and further explore the effectiveness of targeting both androgen biosynthesis and AR activity in combination with other downstream acting agents. AR overexpressing (AR+) TNBC cell lines, xenografts and androgen responsive patient-derived xenograft (PDX) models were using to show how effectively Sevi inhibits AR activity and cell/tumor proliferation. Single cell RNA-sequencing of the AR+ cell line MDA-MB-453 illustrated heterogeneity in AR levels and identified cell cycle pathway activation in ARHigh versus ARLow expressing cells. Combination treatment with the cell cycle CDK4/6 inhibitor abemaciclib and Sevi showed synergy in AR+ TNBC cells and increased effectiveness, compared to each drug alone, in an AR+ TNBC xenograft model. While cell cycle inhibitors have been approved for use in hormone-receptor positive breast cancer, our studies suggest that these drugs may be equally effective in AR+ TNBC cells, especially when combined with AR antagonists. Implications. These data suggest that targeting AR signaling at multiple points throughout the pathway may be an effective was to treat patients with AR+ TNBC.
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