The Brain Immune System: Chemistry and Biology of the Signal Molecules

Galoyan, A. A.

doi:10.1007/978-0-387-30398-7_7

Cited by 10 publications

(7 citation statements)

References 149 publications

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“…PRP-1 was originally isolated from the neurosecretory granules of bovine neurohypophysis. This compound is a cytokine immunomodulator (17), with a wide spectrum of properties (18).…”

Section: Introductionmentioning

confidence: 99%

Restoration of desmosomal junction protein expression and inhibition of H3K9-specific histone demethylase activity by cytostatic proline-rich polypeptide-1 leads to suppression of tumorigenic potential in human chondrosarcoma cells

Galoian

Qureshi

Wideroff

et al. 2014

Molecular and Clinical Oncology

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Abstract. Disruption of cell-cell junctions and the concomitant loss of polarity, downregulation of tumor-suppressive adherens junctions and desmosomes represent hallmark phenotypes for several different cancer cells. Moreover, a variety of evidence supports the argument that these two common phenotypes of cancer cells directly contribute to tumorigenesis. In this study, we aimed to determine the status of intercellular junction proteins expression in JJ012 human malignant chondrosarcoma cells and investigate the effect of the antitumorigenic cytokine, proline-rich polypeptide-1 (PRP-1) on their expression. The cell junction pathway array data indicated downregulation of desmosomal proteins, such as desmoglein (1,428-fold), desmoplakin (620-fold) and plakoglobin (442-fold). The tight junction proteins claudin 11 and E-cadherin were also downregulated (399-and 52-fold, respectively). Among the upregulated proteins were the characteristic for tumors gap junction β-5 protein (connexin 31.1) and the pro-inflammatory pathway protein intercellular adhesion molecule (upregulated 129-and 43-fold, respectively). We demonstrated that PRP-1 restored the expression of the abovementioned downregulated in chondrosarcoma desmosomal proteins. PRP-1 inhibited H3K9-specific histone demethylase activity in chondrosarcoma cells in a dose-dependent manner (0.5 µg/ml PRP, 63%; 1 µg/ml PRP, 74%; and 10 µg/ml PRP, 91% inhibition). Members of the H3K9 family were shown to transcriptionally repress tumor suppressor genes and contribute to cancer progression. Our experimental data indicated that PRP-1 restores tumor suppressor desmosomal protein expression in JJ012 human chondrosarcoma cells and inhibits H3K9 demethylase activity, contributing to the suppression of tumorigenic potential in chondrosarcoma cells.

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“…PRP-1 was originally isolated from the neurosecretory granules of bovine neurohypophysis. This compound is a cytokine immunomodulator (17), with a wide spectrum of properties (18).…”

Section: Introductionmentioning

confidence: 99%

Restoration of desmosomal junction protein expression and inhibition of H3K9-specific histone demethylase activity by cytostatic proline-rich polypeptide-1 leads to suppression of tumorigenic potential in human chondrosarcoma cells

Galoian

Qureshi

Wideroff

et al. 2014

Molecular and Clinical Oncology

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“…The investigation of their biological properties was important step in understanding the molecular mechanisms of immune system and bone marrow regulation [1,2]. The phenomenon of interleukin secretion by hypothalamic magnocellular nuclei as well as biosynthesis of a new class cytokines (PRPs) illustrate the capability of the brain neuroendocrine cells synthesize cytokines along with vasopressin, oxytocin and organotropic (cardioactive) neurohormones.…”

Section: Introductionmentioning

confidence: 99%

Myc-oncogene Inactivating Effect by Proline Rich Polypeptide (PRP-1) in Chondrosarcoma JJ012 Cells

2008

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Proline rich polypeptide (PRP-1) produced by NPV and NSO cells is released into the general circulation and exerts its effect on the activity of immunocompetent and neuronal cells. PRP-1 is a unique regulator of hematopoiesis, stimulator of bone-marrow hematogenesis. Taking into consideration our preliminary data on antitumor and unique diverse biological properties of PRP-1 previously described by Galoyan et al., we proceeded with investigation of the PRP-1 effect on chondrosarcoma, the second most common malignancy in bone, which tends to be locally invasive and then metastatic. Currently it does not have any effective treatment and does not respond either to radiation or chemotherapy, leaving surgical resection as the only option. Our experimental results of PRP-1 action on human chondrosarcoma JJ012 cells demonstrated inactivation, abolishment of Myc oncogene activity usually upregulated in chondrosarcoma cells and other malignancies. The fact that addition of PRP-1 caused drastic inactivation of Myc-luc response element to the control level in human chondrosarcoma JJ012 cell line prompts to investigate further this neuropeptides powerful antioncogenic potential, opening up possibilities to consider PRP-1 as a potential therapeutic tool for chondrosarcoma treatment.

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“…PRP-1 is a cytokine hypothalamic neuropeptide produced by neurosecretory granules of neurohypophysis, in Nucleus supraopticus and Nucleus paraventricularis, the same neurons from which vasopressin and oxytocin originate. PRP-1 is derived from its precursor, neurophysin-vasopressin-associated glycoprotein precursor (20). In addition, large quantities of PRP-1 were detected in bone marrow granulocytes (21).…”

Section: Neuropeptides Involved In Epigenetic Control Of Cancermentioning

confidence: 99%

Epigenetic control of cancer by neuropeptides

Galoian

Patel

2016

Biomedical Reports

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Abstract. Neuropeptides act as neurohormones, neurotransmitters and/or neuromodulators. Neuropeptides maintain physiological homeostasis and are paramount in molecular mechanisms of disease progression and regulation, including in cancer. Neuropeptides, by their definition, originate and are secreted from the neuronal cells, they are able to signal to neighboring cells or are released into the blood flow, if they act as neurohormones. The majority of neuropeptides exert their functions through G protein-coupled receptors, with certain exceptions. Although previous studies indicate that neuropeptides function in supporting proliferation of malignant cells in many types of solid tumor, the antitumorigenic action of the neuropeptides and their receptors, for example, in gastric cancers and chondrosarcoma, were also reported. It is known that epigenetically modified chromatin regulates molecular mechanisms involved in gene expression and malignant progression. The epigenetic modifications are genetically heritable, although they do not cause changes in DNA sequence. DNA methylation, histone modifications and miRNA expression are subject to those modifications. While there is substantial data on epigenetic regulation of neuropeptides, the epigenetic control of cancer by neuropeptides is considered to be uncharted territory. The aim of the current review is to describe the involvement of neuropeptides in the epigenetic machinery of cancer based on data obtained from our laboratory and from other authors.

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The Brain Immune System: Chemistry and Biology of the Signal Molecules

Cited by 10 publications

References 149 publications

Restoration of desmosomal junction protein expression and inhibition of H3K9-specific histone demethylase activity by cytostatic proline-rich polypeptide-1 leads to suppression of tumorigenic potential in human chondrosarcoma cells

Restoration of desmosomal junction protein expression and inhibition of H3K9-specific histone demethylase activity by cytostatic proline-rich polypeptide-1 leads to suppression of tumorigenic potential in human chondrosarcoma cells

Myc-oncogene Inactivating Effect by Proline Rich Polypeptide (PRP-1) in Chondrosarcoma JJ012 Cells

Epigenetic control of cancer by neuropeptides

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