Inhibition of Human Melanoma Growth by a Non-Cardioselective β-Blocker

Wrobel, Ludovic J.; Gal, Frédérique Anne Le

doi:10.1038/jid.2014.373

Cited by 56 publications

(65 citation statements)

References 28 publications

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“…Inhibiting β-adrenergic signaling to pancreatic cancer cells induced apoptosis by suppressing the Ras/Akt/ NFκB signaling pathway [47,48]. Similar findings were also reported in studies of hemangioma, neuroblastoma, melanoma and gastric cancer [49][50][51][52]. Chang et al go as far as to support the use of β-blockers as a possible novel therapeutic intervention, but that claim must be utilized with caution, as recent studies by Wang et al stated that B2 adrenergic stimulation with norepinephrine has actually attenuated invasion of certain types of breast CA's migration [53].…”

Section: Blood Transfusionsupporting

confidence: 70%

Anesthetic Considerations for Management of Cancer Patients to Decrease Cancer Recurrence

Laudański¹,

Wei²,

Korley³

2016

J Anesth Clin Res

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Alongside the known direct, short-term effects of anesthesia in general, there is emerging evidence of an immunomodulatory effect with specific anesthetics that may decrease patient's defences against malignant neoplastic growths. This effect is especially important in the setting of surgical management of neoplasms, which is often the best option for long-term survival in patients with solid neoplasm. Many studies have speculated on the best anesthetic technique to reduce the neoplasm recurrence and promote patient survival, however, we often neglect the sympathetic stress response to neoplasia and how anesthetics modulate this effect. In this review, we study the evidence as it pertains to anesthetic techniques and pain control, particularly general vs. regional anesthesia, and opioid analgesia. At this time there is not enough evidence to support that regional anesthesia has a more favorable outcome than general anesthesia, or that opioids should not be used in neoplasm-related pain management because of their potential pro-metastatic properties secondary to opioid-induced immunosuppression. Instead, the debate over anesthetic use should be centered on adequate pain control since overwhelming evidence have shown that pain-related stress reaction mediated via β-adrenergic activation, promotes neoplastic propagation and metastasis, hence decreasing survival rates.

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Section: Blood Transfusionsupporting

confidence: 70%

Anesthetic Considerations for Management of Cancer Patients to Decrease Cancer Recurrence

Laudański¹,

Wei²,

Korley³

2016

J Anesth Clin Res

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“…PRO, at a concentration of 10 μM, with and without exogenous norepinephrine, significantly reduced proliferation (P < 0.001) and increased apoptosis (P < 0.01) of B16F10 cells compared to controls. Wrobel and Le Gal also showed that PRO had significant effects on proliferation and apoptosis in vitro on a panel of melanoma cell lines at a high concentration of 100 μM [35]. In vivo experiments using both primary and metastatic human melanoma tumours transplanted into immunodeficient (Nod SCID Gamma) mice showed that PRO at an average dose of 1.7 mg/day, tumour volumes were significantly lower (P < 0.001) than in untreated controls.…”

Section: Pre-clinical Evidence In Cancer - In Vitro and In Vivomentioning

confidence: 99%

Repurposing Drugs in Oncology (ReDO)—Propranolol as an anti-cancer agent

Pantziarka

Bouche

Sukhatme³

et al. 2016

ecancer

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Propranolol (PRO) is a well-known and widely used non-selective beta-adrenergic receptor antagonist (beta-blocker), with a range of actions which are of interest in an oncological context. PRO displays effects on cellular proliferation and invasion, on the immune system, on the angiogenic cascade, and on tumour cell sensitivity to existing treatments. Both pre-clinical and clinical evidence of these effects, in multiple cancer types, is assessed and summarised and relevant mechanisms of action outlined. In particular there is evidence that PRO is effective at multiple points in the metastatic cascade, particularly in the context of the post-surgical wound response. Based on this evidence the case is made for further clinical investigation of the anticancer effects of PRO, particularly in combination with other agents. A number of trials are on-going, in different treatment settings for various cancers.

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“…For instance, propranolol, a non-selective β1/2-AR antagonist, reduces melanoma cell proliferation in human and murine melanoma cell lines (Wrobel and Le Gal 2015;Dal Monte et al, 2013). In addition, propranolol reduces tumor growth in a murine model of B16 melanoma (Hasegawa and Saiki 2002;Glasner et al 2010; Barbieri et al 2012).…”

Section: Introductionmentioning

confidence: 98%

Role of host β1- and β2-adrenergic receptors in a murine model of B16 melanoma: functional involvement of β3-adrenergic receptors

Sereni

Monte

Filippi

et al. 2015

Naunyn-Schmiedeberg's Arch Pharmacol

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Complex interactions between tumor cells and their surrounding compartment are strongly influenced by the host in which the tumor grows. In melanoma, for instance, stress-associated norephinephrine (NE), acting at β-adrenergic receptors (β-ARs), stimulates melanoma cell proliferation and tumor angiogenesis. Among β-ARs, β3-ARs play a role acting not only at tumor cells but also at non-neoplastic stromal cells within the melanoma. In the present study, we used a murine model of B16 melanoma to evaluate the role of the host β1- and β2-ARs in melanoma growth and we determined whether the role of β3-ARs can be influenced by the absence of stromal β1- and β2-ARs. As compared to wild-type mice, β1/2-AR knockout mice displayed (i) increased intratumoral levels of both NE and β3-ARs, as evidentiated at both messenger and protein levels; (ii) increased tumor vascularization; (iii) decreased tumor cell proliferation but increased tumor cell apoptosis; and (iv) increased responsiveness to intratumoral injection of the β3-AR blocker L-748,337 in terms of decrease in tumor growth, tumor vascular response, tumor cell proliferation, and increase in tumor cell death. These findings together validate the role of β-AR signaling in melanoma microenvironment suggesting that non-neoplastic stromal cells may be targeted by β-AR-related drugs. The additional fact that β3-ARs play an important role in melanoma growth suggests selective β3-AR antagonists as important proapoptotic agents.

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Inhibition of Human Melanoma Growth by a Non-Cardioselective β-Blocker

Cited by 56 publications

References 28 publications

Anesthetic Considerations for Management of Cancer Patients to Decrease Cancer Recurrence

Anesthetic Considerations for Management of Cancer Patients to Decrease Cancer Recurrence

Repurposing Drugs in Oncology (ReDO)—Propranolol as an anti-cancer agent

Role of host β1- and β2-adrenergic receptors in a murine model of B16 melanoma: functional involvement of β3-adrenergic receptors

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