Imipramine Blue: A potent therapeutic regimen that suppresses breast cancer growth and metastasis
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE72363 | GEO | 2016/08/10
SECONDARY ACCESSION(S): PRJNA293880
REPOSITORIES: GEO
Similar Datasets
Project description:Imipramine Blue a novel inhibitor that we recently synthesiszed suppressed breast cancer growth and progression by silencing FOXM1 and its associated signaling. Breast cancer cell-line MDA-MB-231 treated with vehicle (DMSO) and IB, with 2 biological replciates each.
2016-08-10 | E-GEOD-72363 | biostudies-arrayexpress
Project description: Not available
| S-EPMC4947433 | biostudies-literature
Project description:Rats treated on 7 consecutive days with either 2 injections of vehicle (Ctl) (DMSO for yohimbine, saline for imipramine) or Y+I (2mg/kg Yohimbine + 20mg/kg Imipramine) were sacrificed 2 hours post the last injection and their hippocampi used for gene expression analysis.
2015-12-31 | GSE61301 | GEO
Project description:Glial cells (microglia and astrocytes) have recently became appreciated as an important target for antidepressant drugs. Here we report on the results of comprehensive proteomic analysis of the alteration in protein profile of rat primary mixed glial culture exposed to imipramine. Two-dimensional differential in gel electrophoresis method allowed to identify 62 proteins regulated by imipramine hydrochloride. Functional analysis revealed the impact of imipramine on the level of proteins involved in oxidative stress. Imipramine upregulated proteins related to glycolysis but downregulated many mitochondrial proteins also enzymes of oxidative phosphorylation. Moreover, imipramine influenced the proteins engaged in phagocytosis and cell migration. Alteration in the level of large number of structural and plasma membrane associated proteins evidenced a widespread cytoskeleton and membrane rearrangement. Imipramine triggered decrease of mitochondrial membrane potential, impairment of protein synthesis and downregulation of chaperon proteins, what could be related to increased apoptosis. Many imipramine regulated proteins, among them chaperons, cathepsins and annexins are evidenced to be engaged in immunity response. Overall these experimental findings suggest that in response to imipramine, glial cells (mainly microglia) undergo a transition toward more quiescent, metabolically less demanding phenotype.
2018-05-17 | PXD007977 | Pride
Project description:Rats treated on 7 consecutive days with either 2 injections of vehicle (Ctl) (DMSO for yohimbine, saline for imipramine) or Y+I (2mg/kg Yohimbine + 20mg/kg Imipramine) were sacrificed 2 hours post the last injection and their hippocampi used for gene expression analysis. Agilent one-color experiment,Organism: Rat, Agilent-Rat 8x60k Microarray Gene expression (AMADID: 028279), Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442)
2015-12-31 | E-GEOD-61301 | biostudies-arrayexpress
Project description:Breast cancer is the most common cancer in women and the leading cause of cancer-related deaths in women worldwide. Although survival of breast cancer patients has improved in the last decade, major hurdles remain. Two problems associated with current therapies include acquired resistance and the debilitating side effects of treatment, especially chemotherapy. Therefore, safer treatment options that effectively suppress cancer progression and reduce treatment-associated side effects are much needed. Repurposing of clinically approved or investigational drugs could be one type of effective and safe options for treating cancer patients. Imipramine is a tricyclic antidepressant commonly used for many decades. It is a selective serotonin reuptake inhibitor (SSRI) and inhibits other neurotransmitters. Here, we report that imipramine blocks ER+ and TNBC growth and progression by inhibiting key proteins involved in ER-a signaling, cell cycle progression, and DNA repair and replication. Furthermore, imipramine improved the efficacy of PARP inhibitor therapy in TNBC. This study is the first to show that imipramine is a promising therapeutic option for breast cancer and to define imipramine’s mechanism of action and targets in breast cancer. This pre-clinical study is the basis for a currently ongoing clinical trial testing the efficacy of imipramine for treating breast cancer.
2023-07-06 | GSE190814 | GEO
Project description:Background: Examining transcriptional regulation by existing antidepressants in key neural circuits implicated in depression, and understanding the relationship to transcriptional mechanisms of susceptibility and natural resilience, may help in the search for new therapeutics. Further, given the heterogeneity of treatment response in human populations, examining both treatment response and non-response is critical. Methods: We compared the effects of a conventional monoamine-based tricyclic antidepressant, imipramine (14 daily injections), and a rapidly acting, experimental, non-monoamine-based antidepressant, ketamine (single injection), in mice subjected to chronic social defeat stress, a validated model of depression, and used RNA-sequencing to analyze transcriptional profiles associated with susceptibility, resilience and antidepressant response and non-response in prefrontal cortex (PFC), nucleus accumbens, hippocampus, and amygdala. Results: We identified approximately equal numbers of responder and non-responder mice following ketamine or imipramine treatment. Ketamine induced more expression changes in hippocampus than other brain regions; imipramine induced more expression changes in nucleus accumbens and amygdala. Transcriptional profiles in ketamine and imipramine responders were most similar in PFC, where the least transcriptional regulation occurred for each drug. Non-response reflected both the lack of response-associated gene expression changes and unique gene regulation. In responders, both drugs reversed susceptible associated transcriptional changes as well as induced resilient associated transcription in PFC, with effects varying by drug and brain region studied. Conclusions: We generated a uniquely large resource of gene expression data in four inter-connected limbic brain regions implicated in depression and its treatment with imipramine or ketamine. Our analyses highlight the PFC as a key site of common transcriptional regulation by both antidepressant drugs and in both reversing susceptibility and inducing resilience associated molecular adaptations. In addition, we found region-specific effects of each drug suggesting both common and unique effects of imipramine versus ketamine.
2016-07-27 | GSE81672 | GEO
Project description:The study aim is to evaluate to what extent imipramine treatment of HCT-116 colorectal cell lines does affect fascin1-related or cytoskeleton-associated functions
2020-03-23 | GSE125169 | GEO
Project description:Background: Examining transcriptional regulation by existing antidepressants in key neural circuits implicated in depression, and understanding the relationship to transcriptional mechanisms of susceptibility and natural resilience, may help in the search for new therapeutics. Further, given the heterogeneity of treatment response in human populations, examining both treatment response and non-response is critical. Methods: We compared the effects of a conventional monoamine-based tricyclic antidepressant, imipramine (14 daily injections), and a rapidly acting, experimental, non-monoamine-based antidepressant, ketamine (single injection), in mice subjected to chronic social defeat stress, a validated model of depression, and used RNA-sequencing to analyze transcriptional profiles associated with susceptibility, resilience and antidepressant response and non-response in prefrontal cortex (PFC), nucleus accumbens, hippocampus, and amygdala. Results: We identified approximately equal numbers of responder and non-responder mice following ketamine or imipramine treatment. Ketamine induced more expression changes in hippocampus than other brain regions; imipramine induced more expression changes in nucleus accumbens and amygdala. Transcriptional profiles in ketamine and imipramine responders were most similar in PFC, where the least transcriptional regulation occurred for each drug. Non-response reflected both the lack of response-associated gene expression changes and unique gene regulation. In responders, both drugs reversed susceptible associated transcriptional changes as well as induced resilient associated transcription in PFC, with effects varying by drug and brain region studied. Conclusions: We generated a uniquely large resource of gene expression data in four inter-connected limbic brain regions implicated in depression and its treatment with imipramine or ketamine. Our analyses highlight the PFC as a key site of common transcriptional regulation by both antidepressant drugs and in both reversing susceptibility and inducing resilience associated molecular adaptations. In addition, we found region-specific effects of each drug suggesting both common and unique effects of imipramine versus ketamine. mRNA profiles of susceptibility to chronic social defeat stress as well as treatment response were generated across 4 separate brain regions, with a sample size of 3-5 per group.
2016-07-27 | E-GEOD-81672 | biostudies-arrayexpress
Project description: Not available
| S-EPMC8001973 | biostudies-literature