Norepinephrine Stimulates Pancreatic Cancer Cell Proliferation, Migration and Invasion Via ß-Adrenergic Receptor-Dependent Activation of P38/MAPK Pathway

Huang, Xinyu; Wang, Hongcheng; Zhou, Yuan; Huang, Jinlong; Zheng, Qi

doi:10.5754/hge11476

Cited by 64 publications

(78 citation statements)

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“…Norepinephrine increases the proliferation, migration and invasion of PANC-1 cells, the maximal proliferative effect being induced by the dose of 10 µM (68).…”

Section: Discussionmentioning

confidence: 99%

Catecholamines Increase in Vitro Proliferation of Murine B16F10 Melanoma Cells

Căruntu¹

2014

Acta Endo (Buc)

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Context.Melanoma is the most aggressive skin cancer, with significant morbidity and mortality, and one factor that may influence the course of disease is stress.Objective. Our aim was to evaluate the effect of corticosterone, norepinephrine, epinephrine on murine B16F10 melanoma cells in vitro proliferation.Methods. B16F10 melanoma cells were treated with different concentrations of tested hormones. The proliferative capacity of melanoma cells was quantified by MTS assay and the cell viability was quantified as membrane integrity evaluation measured by lactate dehydrogenase (LDH) release.Results. B16F10 cells treated with corticosterone showed no significant changes. In contrast, norepinephrine exposure stimulated the cell proliferation (P = 0.0003). Treatment with 1 µM norepinephrine induced the highest increase in cell proliferation (OD 492 = 0.27 ± 0.02) statistically significant to both control (OD 492 = 0.17 ± 0.01; p = 0.0003), 10 nM norepinephrine (OD 492 = 0.16 ± 0.00; p = 0.0004) and 100 nM norepinephrine (OD 492 = 0.19 ± 0.01; p = 0.002). Likewise, treatment with epinephrine increased cell proliferation (p = 0.0004). Exposure to 5 µm epinephrine induced a stimulation of cell proliferation (OD 492 = 0.28 ± 0.02) significantly higher compared to controls (OD 492 = 0.17 ± 0.01; p = 0.0004), 50 nM epinephrine (OD 492 = 0.17 ± 0.00; p = 0.001) and 500 nM epinephrine (OD 492 = 0.173 ± 0.00; p = 0.001). Conclusions.Our results may open new perspectives concerning the link between stress hormones and melanoma, emphasizing a direct stimulating in vitro effect induced by catecholamines on melanoma B16F10 cells proliferation.

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“…Norepinephrine increases the proliferation, migration and invasion of PANC-1 cells, the maximal proliferative effect being induced by the dose of 10 µM (68).…”

Section: Discussionmentioning

confidence: 99%

Catecholamines Increase in Vitro Proliferation of Murine B16F10 Melanoma Cells

Căruntu¹

2014

Acta Endo (Buc)

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“…Lin X et al found that the non-selective β-AR agonist isoproterenol significantly increased the activation of ERK/MAPK signal pathway in pancreatic cancer cell [25]. Huang's study showed that norepinephrine also stimulated pancreatic cancer cell proliferation, migration and invasion via β-AR dependent activation of P38/MAPK pathway [34]. Propranolol and other β-blockers reduced the activity of MAPK in pancreatic cancer and Hemangioma [35, 36].…”

Section: Discussionmentioning

confidence: 99%

Propranolol induced G0/G1/S phase arrest and apoptosis in melanoma cells via AKT/MAPK pathway

et al. 2016

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Both preclinical and epidemiology studies associate β-adrenoceptors-blockers (β-blockers) with activity against melanoma. However, the underlying mechanism is still unclear, especially in acral melanoma. In this study, we explored the effect of propranolol, a non-selective β-blocker, on the A375 melanoma cell line, two primary acral melanoma cell lines (P-3, P-6) and mice xenografts. Cell viability assay demonstrated that 50μM-400μM of propranolol inhibited viability in a concentration and time dependent manner with an IC50 ranging from 65.33μM to 148.60μM for 24h −72h treatment, but propranolol (less than 200μM) had no effect on HaCaT cell line. Western blots showed 100μM propranolol significantly reduced the expression of Bcl-2 while increasing the expressions of Bax, cytochrome c, cleaved capase-9 and cleaved caspase-3, and down-regulated the levels of p-AKT, p-BRAF, p-MEK1/2 and p-ERK1/2 in melanoma cells, after a 24h incubation. The in vivo data confirmed the isolation results. Mice received daily ip. administration of propranolol at the dose of 2 mg/kg for 3 weeks and the control group was treated with the same volume of saline. The mean tumor volume at day 21 in A375 xenografts was 82.33 ± 3.75mm3vs. 2044.67 ± 54.57mm3 for the propranolol-treated mice and the control group, respectively, and 31.66 ± 4.67 mm3 vs. 1074.67 ± 32.17 mm3 for the P-3 xenografts. Propranolol also reduced Ki67, inhibited phosphorylation of AKT, BRAF, MEK1/2 and ERK1/2 in xenografts. These are the first data to demonstrate that propranolol might inhibit melanoma by activating the intrinsic apoptosis pathway and inactivating the MAPK and AKT pathways.

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“…Adrenergic receptors are divided into alpha receptors, beta receptors, which are divided into beta 1, beta 2 adrenergic receptor. Recent studies have shown that β-adrenergic receptors were involved in tumor proliferation, invasion, migration and other biological behavioral regulation [7][8][9], and play an important role in tumor progression. The experimental results show that two kinds of beta adrenergic receptors were expressed in glioma cell line LN229 and U251.…”

Section: Discussionmentioning

confidence: 99%

Expression of Beta-Adrenergic Receptor in Glioma LN229 Cells and Its Effect on Cell Proliferation

Dong¹,

Wang²,

Xu³

et al. 2017

Proceedings of the 2016 7th International Conference on Education, Management, Computer and Medicine (EMCM 2016)

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Norepinephrine Stimulates Pancreatic Cancer Cell Proliferation, Migration and Invasion Via ß-Adrenergic Receptor-Dependent Activation of P38/MAPK Pathway

Abstract: NE could stimulate pancreatic cancer cell proliferation, migration and invasion through a β-AR-dependent activation of P38/MAPK pathway involved.

Cited by 64 publications

References 0 publications

Catecholamines Increase in Vitro Proliferation of Murine B16F10 Melanoma Cells

Catecholamines Increase in Vitro Proliferation of Murine B16F10 Melanoma Cells

Propranolol induced G0/G1/S phase arrest and apoptosis in melanoma cells via AKT/MAPK pathway

Expression of Beta-Adrenergic Receptor in Glioma LN229 Cells and Its Effect on Cell Proliferation

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