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Effects of clorgyline, a monoamine oxidase A inhibitor, on high grade prostate cancer cells

ABSTRACT: Monoamine oxidase A (MAO-A), a mitochondrial enzyme that degrades monoamines including neurotransmitters, is highly expressed in basal cells of the normal human prostatic epithelium and in poorly differentiated (Gleason grades 4 and 5), aggressive prostate cancer (PCa). Clorgyline, an MAO-A inhibitor, induces secretory differentiation of normal prostate cells. We systematically assessed gene expression changes induced by clorgyline in E-CA cells using high-density oligonucleotide microarrays. Genes differentially expressed in treated and control cells were identified by Significance Analysis of Microarrays. Expression of genes of interest was validated by quantitative real-time polymerase chain reaction.

ORGANISM(S): Homo sapiens

PROVIDER: GSE17167 | GEO | 2010/07/17

SECONDARY ACCESSION(S): PRJNA119769

REPOSITORIES: GEO

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Effects of clorgyline, a monoamine oxidase A inhibitor, on high grade prostate cancer cells

Project description:Monoamine oxidase A (MAO-A), a mitochondrial enzyme that degrades monoamines including neurotransmitters, is highly expressed in basal cells of the normal human prostatic epithelium and in poorly differentiated (Gleason grades 4 and 5), aggressive prostate cancer (PCa). Clorgyline, an MAO-A inhibitor, induces secretory differentiation of normal prostate cells. We systematically assessed gene expression changes induced by clorgyline in E-CA cells using high-density oligonucleotide microarrays. Genes differentially expressed in treated and control cells were identified by Significance Analysis of Microarrays. Expression of genes of interest was validated by quantitative real-time polymerase chain reaction. time series design

2010-07-17 | E-GEOD-17167 | biostudies-arrayexpress

Monoamine oxidase-dependent pro-survival signaling in diabetic hearts [total RNA]

Project description:Diabetes leads to cardiomyopathy and heart failure, the leading cause of death for diabetic patients. Monoamine oxidase (MAO)-dependent reactive oxygen species (ROS) formation contributes to the development of diabetic cardiomyopathy by inducing mitochondrial and cardiomyocyte dysfunction. Yet, it is unclear whether, in addition to the direct effects exerted by MAO-dependent ROS on mitochondria, MAO activity is able to post-transcriptionally regulate cardiomyocyte function and survival in diabetes. To this aim, we performed gene and miRNA expression profiling in cardiac tissue from a mouse model of type 1 diabetes (T1D) with or without pharmacological MAO inhibition. We found that MAO-dependent ROS generation in T1D hearts leads to profound transcriptomic changes, affecting autophagy and pro-survival pathways activation. MAO activity in T1D hearts affected expression levels of miR-133a-3p, -193a-3p, and -27a-3p that target insulin-like growth factor receptor 1 (Igf1r), growth factor receptor bound protein 10 and inositol polyphosphate 4 phosphatase type 1A, respectively, all components of the Igf1r/PI3K/Akt signaling pathway. Indeed, Akt activation was significantly downregulated in T1D hearts, whereas MAO inhibition restored the activation of this pro-survival pathway. The present study provides an important link between MAO activity, transcriptomic changes, and activation of pro-survival signaling and autophagy in diabetic cardiomyopathy.

2022-09-20 | GSE210611 | GEO

Tranylcypromine specificity for monoamine oxidase is limited by promiscuous protein labelling and lysosomal trapping

Project description:Monoamine oxidases MAOA and MAOB catalyze important cellular functions such as the deamination of neurotransmitters. Correspondingly, MAO inhibitors are used for the treatment of severe neuropsychiatric disorders such as depression. A commonly prescribed drug against refractory depression is tranylcypromine, however, the side effects are poorly understood. In order to decipher putative off-targets, we synthesized two tranylcypromine probes equipped with either an alkyne moiety or an alkyne-diazirine minimal photocrosslinker for in situ proteome profiling. Surprisingly, LC-MS/MS analysis revealed low enrichment of MAOA and relatively promiscuous labeling of proteins. Photoprobe labeling paired with fluorescent imaging studies revealed lysosomal trapping which could be largely reverted by the addition of lysosomotropic drugs.

2020-10-20 | PXD018580 | Pride

Monoamine oxidase-dependent pro-survival signaling in diabetic hearts is mediated by miRNAs

2022-09-20 | GSE210036 | GEO

Monoamine oxidase-dependent pro-survival signaling in diabetic hearts

Project description:Monoamine oxidase-dependent pro-survival signaling in diabetic hearts

| PRJNA866484 | ENA

Novel protein biomarkers of monoamine metabolism defects correlate with disease severity

Project description:Background: Genetic defects of monoamine neurotransmitters are rare neurological diseases amenable to treatment with variable response. They are major causes of early parkinsonism and other spectrum of movement disorders including dopa-responsive dystonia. Objectives: To conduct proteomic studies in cerebrospinal fluid (CSF) samples of patients with monoamine defects to detect biomarkers involved in pathophysiology, clinical phenotypes, and treatment response. Methods: 90 patients from diverse centers of the “International Working Group on Neurotransmitter Related Disorders” were included in the. Clinical and molecular metadata were related to the protein abundances in the CSF. Results: Concentrations of four proteins were significantly altered, detected by Mass spectrometry and confirmed by immunoassays. First, decreased levels of Apolipoprotein D were found in severe cases of aromatic L-amino acid decarboxylase deficiency. Second, low levels of Apolipoprotein H were observed in patients with the severe phenotype of tyrosine hydroxylase deficiency (THD), whereas increased concentrations of oligodendrocyte myelin glycoprotein were found in the same subset of THD patients. Third, decreased levels of Collagen6A3 were observed in treated tetrahydrobiopterin deficiency patients. Conclusion: This study, the largest cohort of patients with monoamine defects studied so far, reports the proteomic characterization of CSF and identify four novel biomarkers that bring new insights into the consequences of early dopaminergic deprivation in the developing brain. They open new possibilities to understand their role in the pathophysiology of these disorders and they may serve as potential predictors of disease severity and therapies.

2020-11-16 | PXD021642 | Pride

Monoamine oxidase-dependent pro-survival signaling in diabetic hearts [total RNA]

Project description:Monoamine oxidase-dependent pro-survival signaling in diabetic hearts [total RNA]

| PRJNA866488 | ENA

SMN deficiency perturbs monoamine neurotransmitter metabolism in spinal muscular atrophy

Project description:<p>Beyond motor neuron degeneration, homozygous mutations in the survival motor neuron 1 (SMN1) gene cause multiorgan and metabolic defects in patients with spinal muscular atrophy (SMA). However, the precise biochemical features of these alterations and the age of onset in the brain and peripheral organs remain unclear. Using untargeted NMR-based metabolomics in SMA mice, we identify cerebral and hepatic abnormalities related to energy homeostasis pathways and amino acid metabolism, emerging already at postnatal day 3 (P3) in the liver. Through HPLC, we find that SMN deficiency induces a drop in cerebral norepinephrine levels in overt symptomatic SMA mice at P11, affecting the mRNA and protein expression of key genes regulating monoamine metabolism, including aromatic L-amino acid decarboxylase (AADC), dopamine beta-hydroxylase (DβH) and monoamine oxidase A (MAO-A). In support of the translational value of our preclinical observations, we also discovered that SMN upregulation increases cerebrospinal fluid norepinephrine concentration in Nusinersen-treated SMA1 patients. Our findings highlight a previously unrecognized harmful influence of low SMN levels on the expression of critical enzymes involved in monoamine metabolism, suggesting that SMN-inducing therapies may modulate catecholamine neurotransmission. These results may also be relevant for setting therapeutic approaches to counteract peripheral metabolic defects in SMA. </p>

2023-11-27 | MTBLS8784 | MetaboLights

Transcriptional analysis of the effect of monoamine oxidase B (MAOB) in human prostate stromal cells (PrSC)

Project description:Transcriptional analysis of the effect of monoamine oxidase B (MAOB) in human prostate stromal cells (PrSC)

| PRJNA778245 | ENA

Therapeutic benefit of rapamycin combined with clorgyline or rasagiline in an immunodeficient LAM model

Project description:Inhibition of mechanistic target of rapamycin (mTOR) constitutes the standard of care of lymphangioleiomyomatosis (LAM). However, this treatment does not eradicate diseased cells and some patients show progressive decline of lung function. This study provides preclinical evidence for beneficial therapeutic approaches in combination with rapamycin. LAM tumorigenesis is reduced in vivo (ELT3-V3 tumor xenografts) using approved drugs for other human diseases and targeting monoamine oxidase A (MAO-A; clorgyline) or MAO-B (rasagiline).

2019-10-01 | GSE129399 | GEO

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