Histamine augments β2-adrenoceptor-induced cyclic AMP accumulation in human prostate cancer cells DU-145 independently of known histamine receptors

Ramos-Jiménez, Judith; Soria-Jasso, Luis-Enrique; López‐Colombo, Aurelio; Reyes‐Esparza, Jorge; Camacho, Javier; Arias‐Montaño, José‐Antonio

doi:10.1016/j.bcp.2006.11.022

Cited by 18 publications

(13 citation statements)

References 41 publications

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“…Histamine proliferating activity was mediated through H1, H2, and H4 receptors and caused the extracellular signal-regulated kinase phosphorylation [72]. In 2007, Ramos-Jiménez et al [73] reported that androgen-independent prostate cancer cells DU-145 express a number of G protein-coupled receptors, including histamine H1 receptors. Tumor necrosis factor-alpha (TNF- α ) was the first cytokine clearly associated with normal MCs in 1990 [74].…”

Section: Mast Cells: a Heterogeneous Cell Populationmentioning

confidence: 99%

Mast Cells as a Potential Prognostic Marker in Prostate Cancer

et al. 2013

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Despite years of intensive investigation that has been made in understanding prostate cancer, it remains one of the major men's health issues and the leading cause of death worldwide. It is now ascertained that prostate cancer emerges from multiple spontaneous and/or inherited alterations that induce changes in expression patterns of genes and proteins that function in complex networks controlling critical cellular events. It is now accepted that several innate and adaptive immune cells, including T- and B-lymphocytes, macrophages, natural killer cells, dendritic cells, neutrophils, eosinophils, and mast cells (MCs), infiltrate the prostate cancer. All of these cells are irregularly scattered within the tumor and loaded with an assorted array of cytokines, chemokines, and inflammatory and cytotoxic mediators. This complex framework reflects the diversity in tumor biology and tumor-host interactions. MCs are well-established effector cells in Immunoglobulin-E (Ig-E) associated immune responses and potent effector cells of the innate immune system; however, their clinical significance in prostate cancer is still debated. Here, these controversies are summarized, focusing on the implications of these findings in understanding the roles of MCs in primary prostate cancer.

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Section: Mast Cells: a Heterogeneous Cell Populationmentioning

confidence: 99%

Mast Cells as a Potential Prognostic Marker in Prostate Cancer

et al. 2013

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“…Recent findings from laboratory models suggest that biobehavioral processes can influence cancer biology via direct effects of the neuroendocrine system on the functional activity of tumor cells (Thaker, Han et al 2006). Many solid epithelial tumors express receptors for neuroendocrine mediators from the sympathetic nervous system (SNS) (the catecholamines, epinephrine and norepinephrine) (Mitra and Carraway 1999;Lutgendorf, Cole et al 2003;Nagmani, Pasco et al 2003;Palm, Lang et al 2006;Thaker, Han et al 2006;Ramos-Jimenez, Soria-Jasso et al 2007;Sastry, Karpova et al 2007) or the hypothalamus-pituitary-adrenal (HPA) axis (the glucocorticoid, cortisol) (Wu, Chaudhuri et al 2004). Analyses carried out in vitro and in mouse xenograft models have shown that neuroendocrine receptors regulate several biological processes involved in cancer metastasis and disease progression, including angiogenesis (Lutgendorf, Cole et al 2003;Thaker, Han et al 2006), tissue invasion (Sood, Bhatty et al 2006;Yang, Sood et al 2006), cell motility (Palm, Lang et al 2006), and programmed cell death (Wu, Chaudhuri et al 2004;Sastry, Karpova et al 2007).…”

Section: Introductionmentioning

confidence: 99%

Depression, social support, and beta-adrenergic transcription control in human ovarian cancer

Lutgendorf

DeGeest

Sung³

et al. 2009

Brain, Behavior, and Immunity

155

157

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Motivated by previous indications that beta-adrenergic signaling can regulate tumor cell gene expression in model systems, we sought to determine whether similar dynamics occur in primary human ovarian cancer. DNA microarray analyses of 10 ovarian carcinomas identified 266 human transcripts that were differentially expressed in tumors from patients with elevated biobehavioral risk factors (high depressive symptoms and low social support) relative to grade-and stage-matched tumors from low-risk patients. Promoter-based bioinformatic analyses confirmed increased activity of several beta-adrenergically-linked transcription control pathways, including CREB/ATF, NF-κB/ Rel, STAT, and Ets family transcription factors. Consistent with increased beta-adrenergic signaling, high biobehavioral risk patients also showed increased intra-tumor concentrations of norepinephrine (but no difference in plasma norepinephrine). These data show that genome-wide transcriptional profiles are significantly altered in patients with high behavioral risk profiles, and they identify betaadrenergic signal transduction as a likely mediator of those differences.

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“…More than 65% of prostate cancers are found in men over 65 years of age, and rarely occurs in men younger than 40 years. Among prostate cancers, the level of plasma testosterone, the stimulant of the androgen receptor, has potent stimulatory effects on androgensensitive parameters in the rat prostate (9). Ramos-Jiménez et al demonstrated that histamine augments β2AR-induced cAMP accumulation in the human prostate cancer cells DU-145 independently of known histamine receptors (9).…”

Section: Introductionmentioning

confidence: 99%

“…Among prostate cancers, the level of plasma testosterone, the stimulant of the androgen receptor, has potent stimulatory effects on androgensensitive parameters in the rat prostate (9). Ramos-Jiménez et al demonstrated that histamine augments β2AR-induced cAMP accumulation in the human prostate cancer cells DU-145 independently of known histamine receptors (9). Additionally, stimulation of endogenous GPCRs in vitro, including those for lysophosphatidic acid (10,11), bombesin (12), and bradykinin (13), induces mitogenic signaling and growth of prostate cancer cells.…”

Section: Introductionmentioning

confidence: 99%

β-arrestin2 mediates β-2 adrenergic receptor signaling inducing prostate cancer cell progression

Zou

2011

Oncol Rep

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Abstract. The expression of the β-2 adrenergic receptor (β2AR), one of the stress-inducible receptors, has been reported to be closely correlated with malignant tumors. Prostate cancer is the most common non-cutaneous cancer among males, accompanied with increased castration levels and β2AR activation in patients. However, the role of β2AR activation in prostate cancer cells and its underlying mechanisms are not fully understood. Here, we found that β2AR activation promoted cell proliferation and cell migration through increasing cellular adenylyl cyclase (cAMP) levels and ERK1/2 activation in LNCaP and PC3 prostate cancer cells. Moreover, the scaffold protein β-arrestin2 was found to be involved in the β2AR-mediated activation of ERK1/2 and cell proliferation using stable overexpressing β-arrestin2 LNCaP (LNCaP-βArr2) cells. Furthermore, enhanced β-arrestin2/ c-Src complex formation by β2AR activation was observed in LNCaP-βArr2 cells. In addition, the c-Src inhibitor could block this enhanced complex formation and suppressed cell proliferation. This study demonstrates that βArr2 is involved in prostate carcinogenesis induced by stress and provides potential therapeutic targets for cancer.

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Histamine augments β2-adrenoceptor-induced cyclic AMP accumulation in human prostate cancer cells DU-145 independently of known histamine receptors

Cited by 18 publications

References 41 publications

Mast Cells as a Potential Prognostic Marker in Prostate Cancer

Mast Cells as a Potential Prognostic Marker in Prostate Cancer

Depression, social support, and beta-adrenergic transcription control in human ovarian cancer

β-arrestin2 mediates β-2 adrenergic receptor signaling inducing prostate cancer cell progression

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