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Pro-metastatic role of catechol-O-methyl transferase in triple negative breast cancer is demonstrated by modulation of cell migration, invasion and cell cycle progression

ABSTRACT: Catechol O-methyl transferase (COMT), a transmembrane protein essential for catechol estrogen detoxification, has been associated with increased migration in triple negative breast cancer (TNBC) in our previous study. Here we studied the role of COMT in TNBC functionally using two clones (B1, D10) of MDA-MB-231 cells with knock-out expression of COMT compared with parental cell line. We performed comparative gene expression analysis using data obtained from RNA-seq of cells with silenced COMT and control cells in biological duplicates.

ORGANISM(S): Homo sapiens

PROVIDER: GSE242452 | GEO | 2025/04/30

REPOSITORIES: GEO

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Catechol-O-methyl transferase suppresses cell invasion and interplays with MET signaling in estrogen dependent breast cancer

Project description:Catechol-O-methyl transferase (COMT) is involved in detoxification of catechol estrogens, playing cancer-protective role in cells producing or utilizing estrogen. Moreover, COMT suppressed migration potential of breast cancer (BC) cells. To delineate COMT role in metastasis of estrogen receptor (ER) dependent BC, we investigated the effect of COMT overexpression on invasion, transcriptome, proteome and interactome of MCF7 cells, a luminal A BC model, stably transduced with lentiviral vector carrying COMT gene (MCF7-COMT). We performed comparative gene expression analysis using data obtained from RNA-seq of COMT-overexpressing and control cells in biological duplicates.

2023-02-01 | GSE203435 | GEO

Catechol-O-methyl transferase suppresses cell invasion and interplays with MET signaling in estrogen dependent breast cancer

Project description:Catechol-O-methyl transferase (COMT) is involved in detoxification of catechol estrogens, playing cancer-protective role in cells producing or utilizing estrogen. Moreover, COMT suppressed migration potential of breast cancer cells. To delineate COMT role in metastasis of estrogen receptor dependent BC, we investigated the effect of COMT overexpression on invasion, transcriptome, proteome and interactome of MCF7 cells, a luminal A breast cancer model, stably transduced with lentiviral vector carrying COMT gene (MCF7-COMT). This PRIDE project includes quantitative analysis results for the total proteome LC-DIA-MS/MS experiment evaluating COMT overexpression in MCF7 breast cancer cell line, and results of pulldown analysis of COMT-interacting proteins in MCF7 cells.

2023-01-31 | PXD033833 | Pride

Integrated multiplexed assays of variant effect reveal determinants of catechol-O-methyltransferase gene expression

Project description:Multiplexed assays of variant effect are powerful methods to profile the consequences of rare variants on gene expression and organismal fitness. Yet, few studies have integrated several multiplexed assays to map variant effects on gene expression in coding sequences. Here, we pioneered a multiplexed assay based on polysome profiling to measure variant effects on translation at scale, uncovering single-nucleotide variants that increase and decrease ribosome load. By combining high-throughput ribosome load data with multiplexed mRNA and protein abundance readouts, we mapped the cis-regulatory landscape of thousands of catechol-O-methyltransferase (COMT) variants from RNA to protein and found numerous coding variants that alter COMT expression. Finally, we trained machine learning models to map signatures of variant effects on COMT gene expression and uncovered both directional and divergent impacts across expression layers. Our analyses reveal expression phenotypes for thousands of variants in COMT and highlight variant effects on both single and multiple layers of expression. Our findings prompt future studies that integrate several multiplexed assays for the readout of gene expression

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Catechol-O-methyl transferase suppresses cell invasion and interplays with MET signaling in estrogen dependent breast cancer

Project description:Catechol-O-methyl transferase suppresses cell invasion and interplays with MET signaling in estrogen dependent breast cancer

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Pro-metastatic role of catechol-O-methyl transferase in triple negative breast cancer is demonstrated by modulation of cell migration, invasion and cell cycle progression

Project description:Pro-metastatic role of catechol-O-methyl transferase in triple negative breast cancer is demonstrated by modulation of cell migration, invasion and cell cycle progression

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Impaired locomotor behavior of C. elegans neuroligin mutants is dependent of the catechol-O-methyltransferase COMT-4

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Traumatic brain injury stimulates hippocampal catechol-O-methyl transferase expression in microglia.

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Gene Expression Data from Prefrontal Cortex and Nucleus Accumbens from Inbred Strains of Mice

Project description:Catechol-O-methyltransferase (COMT) is an ubiquitously expressed enzyme that maintains basic biologic functions by inactivating catechol substrates. In humans, polymorphic variance at the COMT locus has been associated with modulation of pain sensitivity (Andersen & Skorpen, 2009) and risk for developing psychiatric disorders (Harrison & Tunbridge, 2008). A functional haplotype associated with increased pain sensitivity was shown to result in decreased COMT activity by altering mRNA secondary structure-dependent protein translation (Nackley et al., 2006). However, the exact mechanisms whereby COMT modulates pain sensitivity and behavior remain unclear and can be further studied in animal models. We have pursued a genome-wide approach to examining gene expression in multiple brain regions in inbred strains of mice and have discovered that Comt1 is differentially expressed. This expression difference was validated with qPCR. A B2-B4 Short Interspersed Element (SINE) was inserted in the 3'UTR of Comt1 in 14 strains that also shared a common haplotype. Experiments using mammalian expression vectors of full-length cDNA clones with and without the SINE element demonstrate that strains with the SINE haplotype (+SINE) have greater Comt1 enzymatic activity. +SINE mice also exhibit behavioral differences in anxiety assays and decreased pain sensitivity. These results suggest that a haplotype, defined by a 3'UTR B2-B4 SINE element, regulates Comt1 expression and mouse behavior.

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2018-08-29 | GSE119163 | GEO

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