Histamine H<sub>1</sub> receptor activation inhibits the proliferation of human prostatic adenocarcinoma DU‐145 cells

Valencia, Sandra Villacís; Hernández-Angeles, Adriana; Soria-Jasso, Luis-Enrique; Arias‐Montaño, José‐Antonio

doi:10.1002/pros.1096

Cited by 19 publications

(10 citation statements)

References 26 publications

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“…Similarly, loss of SLC18A2 might sensitize prostate cancer cell to the promigratory effects of norepinephrine released from sympathetic nerves (17,18) and/or antiapoptotic stimuli from circulating epinephrine (19), both mediated via h 2 -adrenergic receptors. Histamine, secreted by infiltrating mast cells, augments h 2 -adrenergic receptormediated responses in prostate cancer cells in vitro independent of the H1 receptor (44) but has also been shown to inhibit proliferation via the H1 receptor (16). Finally, perineural invasion is regarded as a key mechanism for prostate cancer spreading, where neurons in the prostate seem to be a source for tumor-promoting paracrine factors, leading to reduced apoptosis and increased proliferation of nearby prostate cancer cells (45).…”

Section: Discussionmentioning

confidence: 99%

“…Although murine knockout models have disclosed important biological roles of SLC18A2 in the nervous system (10 -12), its possible function in normal and malignant prostate biology remains unknown. However, several of the monoamines that are substrates for SLC18A2-mediated transport have been shown to influence growth (13 -15), proliferation (16), migration (17,18), or apoptosis (19) of prostate cancer cells in vitro and in vivo.…”

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confidence: 99%

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Genetic and Epigenetic SLC18A2 Silencing in Prostate Cancer Is an Independent Adverse Predictor of Biochemical Recurrence after Radical Prostatectomy

Sørensen¹,

Wild

Mortezavi

et al. 2009

Clinical Cancer Research

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Purpose: This study investigates SLC18A2 (vesicular monoamine transporter 2) expression in prostate adenocarcinoma and examines its potential as a predictive marker for prostate cancer patient outcome after radical prostatectomy. Experimental Design: Expression and single nucleotide polymorphism microarray analyses identified SLC18A2 as both down-regulated and subject to common loss-of-heterozygosity in prostate cancer. Down-regulated SLC18A2 expression was validated on tissue microarrays containing benign and malignant prostate specimens from an independent patient group (n = 738). Furthermore, SLC18A2 immunoreactivity in radical prostatectomy tumor specimens (n = 506) was correlated to clinicopathologic characteristics and recurrence-free survival. The possibility of SLC18A2 silencing by aberrant DNA methylation in prostate cancer cells was investigated by bisulfite sequencing. Results: Tissue microarray analysis revealed markedly lower cytoplasmic SLC18A2 staining in cancer compared with nonmalignant prostate tissue samples, confirming RNA expression profiling results. Furthermore, multivariate analysis identified cytoplasmic SLC18A2 immunoreactivity as a novel predictor of biochemical recurrence following prostatectomy (hazard ratio, 0.485; 95% confidence interval, 0.333-0.709; P < 0.001) independent of prostate-specific antigen, Gleason score, tumor stage, and surgical margin status. SLC18A2 showed loss-of-heterozygosity in 23% of the tumors and was densely hypermethylated in 15 of 17 (88%) prostate cancer samples plus 6 of 6 prostate cancer cell lines. In contrast, SLC18A2 was unmethylated in 4 of 4 adjacent nonmalignant prostate and 3 of 5 benign prostatic hyperplasia tissue samples, whereas 2 of 5 benign prostatic hyperplasia samples had monoallelic hypermethylation. Methylation and histone deacetylase inhibitory agents rescued SLC18A2 expression in three prostate cancer cell lines. Conclusions: SLC18A2 silencing by DNA hypermethylation and/or allelic loss is a frequent event inprostate cancerandanovelindependent predictorofbiochemicalrecurrenceafterprostatectomy.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Genetic and Epigenetic SLC18A2 Silencing in Prostate Cancer Is an Independent Adverse Predictor of Biochemical Recurrence after Radical Prostatectomy

Sørensen¹,

Wild

Mortezavi

et al. 2009

Clinical Cancer Research

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“…Recently, it has been suggested that mast cells influence the proliferation of cancer cells and promote the invasion of cancer cells by reorganizing the cancer cell's microenvironment and modulating immune responses to cancer cells. Mast cells induce the migration of T-cells and antigen-presenting dendritic cells and subsequently may affect cancer cell functions [152]. In addition, other cells such as eosinophilic granulocytes, dentritic cells, and T-cells may also contribute to cancer cell stimulation that induces the onset of invasiveness and epigenetic alterations for a certain type of cancer cells [152,154].…”

Section: Effect Of Adjacent Cells (Non-endothelial Cells) On Cancer Cmentioning

confidence: 99%

“…Previously, it has been reported that histamine released by mast cells upon stimulation, increases the stiffness of histamine receptor presenting cells such as endothelial cells [147]. Thus, several cancer cells types possess also histamine receptors [148][149][150][151] and might be stimulated by mast cells that are frequently found in the neighborhood of tumor masses [152,153]. Until now, the function of mast cells within these tumors or in their close neighborhood remains to be unclear.…”

Section: Effect Of Adjacent Cells (Non-endothelial Cells) On Cancer Cmentioning

confidence: 99%

The Biomechanical Properties of 3d Extracellular Matrices and Embedded Cells Regulate the Invasiveness of Cancer Cells

Mierke

2011

Cell Biochem Biophys

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The malignancy of tumors depends on the biomechanical properties of cancer cells and their microenvironment, which enable cancer cells to migrate through the connective tissue, transmigrate through basement membranes and endothelial monolayers and form metastases in targeted organs. The current focus of cancer research is still based on biological capabilities such as molecular genetics and gene signaling, but these approaches ignore the mechanical nature of the invasion process of cancer cells. This review will focus on how structural, biochemical and mechanical properties of extracellular matrices (ECMs), and adjacent cells regulate the invasiveness of cancer cells. In addition, it presents how cancer cells create their own microenvironment by restructuring of the ECM and by interaction with stromal cells, which then further contribute to the progression of cancer disease. Finally, this review will point out that mechanical properties are a critical determinant for the efficiency of cancer cell invasion and the progression of cancer which might affect the future development of new cancer treatments.

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“…Furthermore, elevated expression of the HRH1 gene has been shown to be associated with poor survival for both lung cancer and B-cell lymphoma patients (70). Several other studies demonstrated that H1R activation suppressed cell proliferation in prostate cancer (67), melanoma (40), and leukemia (31) cells and promoted cell migration of cervical carcinoma cells (57). Altogether, the effects of histamine-receptor activation seem to be tissue specific, depending on relative distributions of histamine receptors in different tissue types (37).…”

Section: Introductionmentioning

confidence: 99%

Distinct roles of histamine H1- and H2-receptor signaling pathways in inflammation-associated colonic tumorigenesis

Shi

Fultz

Engevik

et al. 2019

American Journal of Physiology-Gastrointestinal and Liver Physi

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Inflammatory bowel disease (IBD) is a well-known risk factor for the development of colorectal cancer. Prior studies have demonstrated that microbial histamine can ameliorate intestinal inflammation in mice. We tested the hypothesis whether microbe-derived luminal histamine suppresses inflammation-associated colon cancer in Apcmin/+ mice. Mice were colonized with the human-derived Lactobacillus reuteri. Chronic inflammation was induced by repeated cycles of low-dose dextran sulfate sodium (DSS). Mice that were given histamine-producing L. reuteri via oral gavage developed fewer colonic tumors, despite the presence of a complex mouse gut microbiome. We further demonstrated that administration of a histamine H1-receptor (H1R) antagonist suppressed tumorigenesis, while administration of histamine H2-receptor (H2R) antagonist significantly increased both tumor number and size. The bimodal functions of histamine include protumorigenic effects through H1R and antitumorigenic effects via H2R, and these results were supported by gene expression profiling studies on tumor specimens of patients with colorectal cancer. Greater ratios of gene expression of H2R ( HRH2) vs. H1R ( HRH1) were correlated with improved overall survival outcomes in patients with colorectal cancer. Additionally, activation of H2R suppressed phosphorylation of mitogen-activated protein kinases (MAPKs) and inhibited chemokine gene expression induced by H1R activation in colorectal cancer cells. Moreover, the combination of a H1R antagonist and a H2R agonist yielded potent suppression of lipopolysaccharide-induced MAPK signaling in macrophages. Given the impact on intestinal epithelial and immune cells, simultaneous modulation of H1R and H2R signaling pathways may be a promising therapeutic target for the prevention and treatment of inflammation-associated colorectal cancer. NEW & NOTEWORTHY Histamine-producing Lactobacillus reuteri can suppress development of inflammation-associated colon cancer in an established mouse model. The net effects of histamine may depend on the relative activity of H1R and H2R signaling pathways in the intestinal mucosa. Our findings suggest that treatment with H1R or H2R antagonists could yield opposite effects. However, by harnessing the ability to block H1R signaling while stimulating H2R signaling, novel strategies for suppression of intestinal inflammation and colorectal neoplasia could be developed.

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Histamine H₁ receptor activation inhibits the proliferation of human prostatic adenocarcinoma DU‐145 cells

Abstract: Histamine inhibits the proliferation of DU-145 cells through the activation of H(1) receptors coupled to phosphoinositide hydrolysis.

Cited by 19 publications

References 26 publications

Genetic and Epigenetic SLC18A2 Silencing in Prostate Cancer Is an Independent Adverse Predictor of Biochemical Recurrence after Radical Prostatectomy

Genetic and Epigenetic SLC18A2 Silencing in Prostate Cancer Is an Independent Adverse Predictor of Biochemical Recurrence after Radical Prostatectomy

The Biomechanical Properties of 3d Extracellular Matrices and Embedded Cells Regulate the Invasiveness of Cancer Cells

Distinct roles of histamine H1- and H2-receptor signaling pathways in inflammation-associated colonic tumorigenesis

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Histamine H1 receptor activation inhibits the proliferation of human prostatic adenocarcinoma DU‐145 cells

Abstract: Histamine inhibits the proliferation of DU-145 cells through the activation of H(1) receptors coupled to phosphoinositide hydrolysis.

Cited by 19 publications

References 26 publications

Genetic and Epigenetic SLC18A2 Silencing in Prostate Cancer Is an Independent Adverse Predictor of Biochemical Recurrence after Radical Prostatectomy

Genetic and Epigenetic SLC18A2 Silencing in Prostate Cancer Is an Independent Adverse Predictor of Biochemical Recurrence after Radical Prostatectomy

The Biomechanical Properties of 3d Extracellular Matrices and Embedded Cells Regulate the Invasiveness of Cancer Cells

Distinct roles of histamine H1- and H2-receptor signaling pathways in inflammation-associated colonic tumorigenesis

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Histamine H₁ receptor activation inhibits the proliferation of human prostatic adenocarcinoma DU‐145 cells