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Antiandrogen Flutamide-Induced Restoration of miR-449 Expression Mitigates Molecular Markers Associated with Ovarian Cancer Risk

ABSTRACT: Antiandrogen Flutamide-Induced Restoration of miR-449 Expression Mitigates Molecular Markers Associated with Ovarian Cancer Risk

PROVIDER: PRJNA1058012 | ENA |

REPOSITORIES: ENA

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Antiandrogen Flutamide-Induced Restoration of miR-449 Expression Mitigates Molecular Markers Associated with Ovarian Cancer Risk

Project description:The involvement of the androgen receptor (AR) pathway in the development of epithelial ovarian cancer is increasingly recognized. We examined the effects of the anti-androgen agent flutamide on miRNA expression in women at high risk (HR) for ovarian cancer. Flutamide treatment restored the reduced expression of miR-449a and miR-449b-5p in HR tissues, thereby decreasing CSF1R and AR expression associated with an increased risk of ovarian cancer. In addition to the known direct binding of flutamide to the AR, we found that flutamide also suppresses AR expression via miR-449a and miR-449b-5p upregulation, revealing a novel dual-inhibitory mechanism on the AR pathway. Taken together, our study highlights the chemopreventive potential of flutamide in ovarian cancer and suggests avenues for future research and clinical applications.

2024-12-18 | GSE252170 | GEO

Transcription profiling by array of mouse pachytene cells from mir-34bc+/-;449+/- and mir-34bc-/-;449-/- male animals.

Project description:Analysis of gene expression (mRNA profiles) from mouse pachytene cells. Mir-34bc+/-;449+/- samples are compared against mir-34bc-/-;449-/- samples .

2014-08-17 | E-MTAB-2668 | biostudies-arrayexpress

Rhizobium leguminosarum strain:SEMIA 449 | isolate:SEMIA 449

Project description:Rhizobium leguminosarum SEMIA 449 genome sequencing

| PRJNA581060 | ENA

Firmicutes bacterium CAG:449

Project description:Firmicutes bacterium CAG:449 overview

| PRJNA207242 | ENA

Rb and p53 cooperate to suppress prostate cancer lineage plasticity, metastasis, and antiandrogen resistance

Project description:Prostate cancer relapsing from antiandrogen therapies can exhibit variant histology with altered lineage marker expression, suggesting lineage plasticity facilitates therapeutic resistance. Mechanisms underlying prostate cancer lineage plasticity are unknown, and relevant experimental models are needed. We demonstrate Rb1 loss facilitates lineage plasticity and metastasis of prostate adenocarcinoma initiated by Pten mutation in the mouse. Additional loss of Trp53 causes resistance to antiandrogen therapy. Gene expression profiling indicates mouse tumors are comparable to human prostate cancer neuroendocrine variants; both mouse and human tumors exhibit increased expression of epigenetic reprogramming factors like Ezh2 and Sox2. Clinically relevant Ezh2 inhibitors restore androgen receptor expression and sensitivity to antiandrogen therapy. These findings uncover genetic mutations enabling prostate cancer progression, identify mouse models for studying prostate cancer lineage plasticity, and suggest an epigenetic approach for extending clinical responses to antiandrogen therapy.

2017-02-24 | GSE90891 | GEO

Pseudomonas sp. MOB-449

Project description:Pseudomonas sp. MOB-449 Genome sequencing and assembly

| PRJNA851417 | ENA

Populus trichocarpa strain:Besc-449

Project description:Populus trichocarpa strain:Besc-449 Genome sequencing

| PRJNA250349 | ENA

Transcriptomic impact of microRNAs-449 or microRNAs-34 overexpression in proliferating human airway epithelial cells

Project description:We used microarrays to detail the global programme of gene expression that occurs in response to miR-449 or miR-34 overexpression in proliferating HAECs.

2011-06-07 | GSE22143 | GEO

Effects of trenbolone, flutamide and a mix of both in fathead minnow ovaries

Project description:Trenbolone and flutamide are prototypical model compounds for respectively androgen and anti-androgen modes of action. Trenbolone is an anabolic steroid used in cattle industry to increase weight gain and feed efficiency, and flutamide is a pharmaceutical used to treat prostate cancer. Androgens exert profound effects on the organization, development, and function of the male reproductive system through activation of androgen receptors (ARs). Flutamide, as an antiandrogen, was expected to temper the effects of trenbolone on androgen receptor (AR)-mediated gene expression. Female fathead minnows (Pimephales promelas) were exposed via the water to 0.05, 0.5 or 5 µg 17β-trenbolone/L; 50, 150 or 500 µg flutamide/L; or to a mixture of 0.5 μg/L trenbolone and 500 μg/L flutamide. After a 48 hr constant exposure gene expression in gonads was analyzed using a fathead minnow-specific 22,000-gene microarray. Trenbolone significantly changed the expression (P < 0.05) of roughly 750 different genes, while flutamide changed the expression of 1420 genes. Most of the genes that were regulated were distinct for the two chemicals. However, 70 genes were reciprocally regulated by the two treatments. Myelocytomatosis viral oncogene homolog (Myc), Yin Yang 1 (YY1) and interferon regulator factor 1 (IRF1) were among the important transcription factors reciprocally regulated by trenbolone and flutamide, suggesting they may be specifically regulated by the AR. These regulatory molecules, in conjunction with other reciprocally regulated transcription factors, may function as early molecular switches to control phenotypic changes in gonad tissue architecture and function. Fathead minnows exposed for 48h to 0.5 ug trenbolone, 500 ug flutamide, or a mixture of both.

2008-12-23 | E-GEOD-14100 | biostudies-arrayexpress

Exercise Mitigates Skeletal Muscle Epigenetic Aging

Project description:Exercise late in life mitigates skeletal muscle epigenetic aging, providing evidence that physical activity is a "fountain of youth".

2021-12-31 | GSE175410 | GEO

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