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LncRNA LOC730101 promotes darolutamide resistance in prostate cancer by suppressing miR-1-3p [RNA-Seq]

ABSTRACT: This study investigates the role of noncoding RNAs in resistance to the anti-androgen drug daro-lutamide in prostate cancer. RNA sequencing identified LOC730101 as a significantly elevated lncRNA in darolutamide-resistant cells. Silencing LOC730101 reduced cell proliferation, indicating its role in drug resistance.

ORGANISM(S): Homo sapiens

PROVIDER: GSE269645 | GEO | 2024/08/15

REPOSITORIES: GEO

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LncRNA LOC730101 promotes darolutamide resistance in prostate cancer by suppressing miR-1-3p [Hi-C]

Project description:This study investigates the role of noncoding RNAs in resistance to the anti-androgen drug daro-lutamide in prostate cancer. RNA sequencing identified LOC730101 as a significantly elevated lncRNA in darolutamide-resistant cells. Silencing LOC730101 reduced cell proliferation, indicating its role in drug resistance.

2024-08-15 | GSE269644 | GEO

Darolutamide antagonizes androgen signaling by blocking enhancer and super-enhancer activation [RNA-seq]

Project description:The androgen receptor (AR) antagonist darolutamide has very recently been approved for the treatment of non-metastatic castration resistant prostate cancer (PCa). Here we determined the genome-wide effects of darolutamide on cis-acting regulatory elements involved in androgen signaling with a focus on enhancer and super-enhancer (SE) regions. Darolutamide strongly depleted the AR from regulatory elements and abolished the AR transcriptional signaling. Using two different androgen-dependent PCa cell lines we identified genomic-regions with different affinities for the AR in androgen-stimulated, androgen-depleted and darolutamide-antagonized conditions. Altogether, our findings demonstrate that darolutamide is a potent AR antagonist blocking genome-wide AR signaling and AR enhancer activation. Further, we show a dynamic AR cistrome and concomitant adapting chromatin environment to varying conditions and identified regions with high AR affinity in cell lines and tissue samples.

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Darolutamide antagonizes androgen signaling by blocking enhancer and super-enhancer activation [ChIP-seq]

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LncRNA LOC730101 promotes darolutamide resistance in prostate cancer by suppressing miR-1-3p [Hi-C]

Project description:LncRNA LOC730101 promotes darolutamide resistance in prostate cancer by suppressing miR-1-3p [Hi-C]

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LncRNA LOC730101 promotes darolutamide resistance in prostate cancer by suppressing miR-1-3p [RNA-Seq]

Project description:LncRNA LOC730101 promotes darolutamide resistance in prostate cancer by suppressing miR-1-3p [RNA-Seq]

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Comparative proteomic and transcriptomic analysis of the impact of androgen stimulation and darolutamide inhibition on prostate cancer cells

Project description:Androgen receptor (AR) signaling is a major driver and therapy target in prostate cancer. Several inhibitors of AR function are approved for different stages of the disease and their impact on downstream gene transcription has been described. However, the ensuing effects of androgen and anti-androgens at the protein level are less well understood. Here, we focused on the AR inhibitor darolutamide which has recently been approved for non-metastatic castration-resistant prostate cancer. Here we determined the impact of darolutamide, a recently approved AR antagonist which significantly extends progression-free and overall survival in non-metastatic CRPC (31, 32), on the prostate cancer proteome. We first determined the direct binding between darolutamide and the AR in living prostate cancer cells in a label-free context using the cellular high throughput thermal shift assay (CETSA HT). We then generated comprehensive proteomic profiles of prostate cancer cells treated with androgen and darolutamide, and compared them with transcriptomic profiles. We found a generally high concordance between proteomic and transcriptomic data, both on the level of detected expressed genes and their protein products, as well as in terms of the corresponding biological programs. However there were cases where protein and gene expression levels were not regulated in parallel, suggesting an additional post-transcriptional regulation step controlling protein abundance to occur in several instances.

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Darolutamide antagonizes androgen signaling by blocking enhancer and super-enhancer activation

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Darolutamide antagonizes androgen signaling by blocking enhancer and super-enhancer activation [ChIP-seq]

Project description:Darolutamide antagonizes androgen signaling by blocking enhancer and super-enhancer activation [ChIP-seq]

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Darolutamide antagonizes androgen signaling by blocking enhancer and super-enhancer activation [RNA-seq]

Project description:Darolutamide antagonizes androgen signaling by blocking enhancer and super-enhancer activation [RNA-seq]

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Dual targeting of the androgen receptor and PI3K/AKT/mTOR pathways in prostate cancer elicits improved anti-tumor efficacy and apoptosis

Project description:Both the PI3K/AKT/mTOR and androgen receptor (AR) signaling pathways play essential roles in prostate cancer. We compared the impact of PI3K/AKT/mTOR pathway inhibitors with different selectivity profiles on in vitro cell proliferation and apoptosis induction, and observed the strongest effects in androgen-sensitive prostate cancer models. Combination treatment with the AR inhibitor darolutamide led to enhanced apoptosis in these cell lines, with most pronounced effects of the pan-PI3K inhibitor copanlisib. Transcriptomic analysis performed in the androgen-sensitive VCaP cell line revealed that gene expression was more affected by the co-treatment with darolutamide and copanlisib, compared to single agents. A comprehensive reversal of the androgen response and the mTORC1 transcriptional programs was observed. The combination treatment also markedly induced DNA damage. An in vivo efficacy study performed using LuCaP 35, an androgen-sensitive patient-derived prostate cancer model, indicated superior efficacy after combined treatment with copanlisib and darolutamide. Immunohistochemistry analysis of treated tumors furthermore showed increased apoptosis. Altogether these data demonstrate that blocking the PI3K/AKT/mTOR and AR pathways with potent inhibitors has superior anti-tumor efficacy and induces apoptosis in androgen-sensitive prostate cancer models.

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