Differential effects of methionine enkephalin on the growth of brain tumor cells

Lee, Yong Soo; Wurster, Robert D.

doi:10.1007/bf01051044

Cited by 16 publications

(8 citation statements)

References 23 publications

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“…1998). The ability to stimulate either traditional opioid signalling pathways (see Huang 1995) and/or MAP‐kinase may explain how opioids can have varied effects on cell division (Lee & Wurster 1994; Law & Bergsbaken 1995; Hauser & Mangoura 1998; Knapp et al . 1998).…”

Section: Discussionmentioning

confidence: 99%

Opioids intrinsically inhibit the genesis of mouse cerebellar granule neuron precursors in vitro: differential impact of μ and δ receptor activation on proliferation and neurite elongation

Hauser

Houdi

Turbek

et al. 2000

Eur J of Neuroscience

103

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Although opioids are known to affect neurogenesis in vivo, it is uncertain the extent to which opioids directly or indirectly affect the proliferation, differentiation or death of neuronal precursors. To address these questions, the intrinsic role of the opioid system in neurogenesis was systematically explored in cerebellar external granular layer (EGL) neuronal precursors isolated from postnatal mice and maintained in vitro. Isolated neuronal precursors expressed proenkephalin-derived peptides, as well as specific mu and delta, but negligible kappa, opioid receptors. The developmental effects of opioids were highly selective. Morphine-induced mu receptor activation inhibited DNA synthesis, while a preferential delta2-receptor agonist ([D-Ala2]-deltorphin II) or Met-enkephalin, but not the delta1 agonist [D-Pen2, D-Pen5]-enkephalin, inhibited differentiation within the same neuronal population. If similar patterns occur in the developing cerebellum, spatiotemporal differences in endogenous mu and delta opioid ligand-receptor interactions may coordinate distinct aspects of granule neuron maturation. The data additionally suggest that perinatal exposure to opiate drugs of abuse directly interfere with cerebellar maturation by disrupting normal opioid signalling and inhibiting the proliferation of granule neuron precursors.

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Section: Discussionmentioning

confidence: 99%

Opioids intrinsically inhibit the genesis of mouse cerebellar granule neuron precursors in vitro: differential impact of μ and δ receptor activation on proliferation and neurite elongation

Hauser

Houdi

Turbek

et al. 2000

Eur J of Neuroscience

103

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“…Met 5 enkephalin has dual effects on tumor cell growth. This peptide exerted an inhibitory effect in SK-N-MC human neuroblastoma cell line; in contrast, it stimulates the growth of U-373 MG human astrocytoma cell line (103). Beta casomorphine-5, and DAMGO stimulated neurite outgrowth, while DPDPE and U-50488, a kappa agonist, had no effect (104).…”

Section: Opioids and Somatostatin In Cancer Cell Proliferationmentioning

confidence: 94%

Opioid-somatostatin interactions in regulating cancer cell growth

Hatzoglou¹

2005

Front Biosci

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Opioids and somatostatin mediate their cellular effects through specific membrane receptors. Three major receptor classes (delta, mu and kappa) were identified for opioids, while for somatostatin, five different receptor classes (SSTR1-5) have been cloned. Through the interaction with their receptors, opioids and somatostatin exert their effects on cell growth, proliferation, differentiation and secretion. Specific actions of each receptor type have been reported, to be implicated in one or more of the cell functions referred above but have been mainly correlated with cell growth control. In several systems the effect of either neuropeptide is the reverse, inducing cell growth rather than antiproliferative and proapoptotic signals. In recent years, a growing number of reports indicate a possible interaction between opioid and somatostatin system. This could occur at the receptor level, through a cross-interaction of either neuropeptide with either receptor type, or receptor hetero-dimerization, and at a post-receptor level, via interaction with specific signaling molecules. These interactions provide new directions for the identification of specific molecules acting at the receptor and post-receptor level, mimicking the effects of both categories of agents.

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“…RHAMM isoforms are involved in regulation of extracellular signal-regulated kinase (ERK) activity (Zhang et al, 1998), a protein kinase activated in response to a variety of growth factors. The expression of preproenkephalin is higher in dividing cells than in confluent cells (Hildebrand et al, 1997) and Met-enkephalin stimulated the growth of astrocytoma cells (Lee and Wurster, 1994). S-100 42A has been shown to control cell cycle progression via sequestration and inactivation of p53 (reviewed in a Relative P bins were converted to absolute P-false values as described .…”

Section: Discussionmentioning

confidence: 99%

Growth and migration markers of rat C6 glioma cells identified by serial analysis of gene expression

Gunnersen

Spirkoska

Smith

et al. 2000

Glia

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Differential effects of methionine enkephalin on the growth of brain tumor cells

Cited by 16 publications

References 23 publications

Opioids intrinsically inhibit the genesis of mouse cerebellar granule neuron precursors in vitro: differential impact of μ and δ receptor activation on proliferation and neurite elongation

Opioids intrinsically inhibit the genesis of mouse cerebellar granule neuron precursors in vitro: differential impact of μ and δ receptor activation on proliferation and neurite elongation

Opioid-somatostatin interactions in regulating cancer cell growth

Growth and migration markers of rat C6 glioma cells identified by serial analysis of gene expression

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