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Targeting NK-1 Receptors to Prevent and Treat Pancreatic Cancer: a New Therapeutic Approach

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Targeting NK-1 Receptors to Prevent and Treat Pancreatic Cancer: a New Therapeutic Approach Cancers 2015, 7, 1215-1232; doi:10.3390/cancers7030832 cancersOPEN ACCESS ISSN 2072-6694 www.mdpi.com/journal/cancers Review Targeting NK-1 Receptors to Prevent and Treat Pancreatic Cancer: a New Therapeutic Approach Miguel Muñoz 1;* and Rafael Coveñas 2 1 Research Laboratory on Neuropeptides (IBIS), Virgen del Rocío University Hospital, 41013 Sevilla, Spain 2 Laboratory of Neuroanatomy of the Peptidergic System (Lab. 14), Institute of Neurosciences of Castilla y León (INCYL), University of Salamanca, 37008 Salamanca, Spain; E-Mail: [email protected] * Author to whom correspondence should be addressed; E-Mail: [email protected]; Tel.: +34-955-012-965; Fax: +34-955-012-921. Academic Editor: Hildegard M. Schuller Received: 19 May 2015 / Accepted: 30 June 2015 / Published: 6 July 2015 Abstract: Pancreatic cancer (PC) is the fourth leading cause of cancer related-deaths in both men and women, and the 1- and 5-year relative survival rates are 25% and 6%, respectively. It is known that smoking, alcoholism and psychological stress are risk factors that can promote PC and increase PC progression. To date, the prevention of PC is crucial because there is no curative treatment. After binding to the neurokinin-1 (NK-1) receptor (a receptor coupled to the stimulatory G-protein Gαs that activates adenylate cyclase), the peptide substance P (SP)—at high concentrations—is involved in many pathophysiological functions, such as depression, smoking, alcoholism, chronic inflammation and cancer. It is known that PC cells and samples express NK-1 receptors; that the NK-1 receptor is overexpressed in PC cells in comparison with non-tumor cells, and that nanomolar concentrations of SP induce PC cell proliferation. By contrast, NK-1 receptor antagonists exert antidepressive, anxiolytic and anti-inflammatory effects and anti-alcohol addiction. These antagonists also exert An antitumor action since in vitro they inhibit PC cell proliferation (PC cells death by apoptosis), and in a xenograft PC mouse model they exert both antitumor and anti-angiogenic actions. NK-1 receptor antagonists could be used for the treatment of PC and hence the NK-1 receptor could be a new promising therapeutic target in PC. Cancers 2015, 7 1216 Keywords: substance P; NK-1 receptor antagonist; chronic pancreatitis; inflammation; smoking; alcoholism; depression 1. Introduction Pancreatic cancer (PC), one of the most ominous types of cancer, is the fourth leading cause of cancer related-deaths in both men and women, with less than 5% survival at 5 years after diagnosis. In 2013, the American Cancer Society estimated that there were 45,220 new cases of PC in the United States and 38,460 deaths from the disease. Treatment strategies have not succeeded in significantly extending patient survival, and clinical outcome has not improved substantially over the past 35 years; the overall 5-year survival rate remains dismal, around 5% [1]. Thus, PC continues to be a major unsolved health problem and conventional treatments unfortunately have little impact on the course of the disease. Almost all patients suffering from PC develop metastases, this being the main reason for its lethality [2]. Cytostatic drugs show a low safety profile and severe side effects (e.g., anaemia, leukopenia), because these drugs are not specific against cancer cells. Currently, due to having the worst prognosis, a lack of early diagnostic symptoms, and resistance to conventional chemo- and radiotherapies, PC remains a very complex malignancy. Thus, because there is still a lack of curative therapy there is An urgent need to prevent PC by applying new strategies and/or by improving current therapies [3]. Research into this issue should focus on drugs with fewer side effects than those produced by cytostatic drugs and this can only be achieved if the drug is specific against PC cells. In light of the above, a better understanding of both etiology and early developmental events in PC is vital. The evolution of advanced PC from initial pancreatic injury is a multi-factorial phenomenon involving a series of sequential events. The initial acute infection or tissue damage triggers inflammation, initiating the process of establishing a state of homeostasis in conjunction with innate immunity, aimed at limiting harm to the body. Upon recurrent pancreatic injuries, which may be due to genetic susceptibility, smoking and alcohol abuse, unhealthy diet, a pro-inflammatory milieu is induced; comprising several types of immune cells, growth factors, chemokines, cytokines and restructured extracellular matrix; this leads to prolonged inflammatory/chronic conditions [4]. Cells that have sustained DNA damage and/or mutagenic assault exploit the prolonged inflammatory response aiding in the initiation and development of neoplastic/fibrotic events. Many tumor-stromal interactions result in a chaotic environment, where loss of immune surveillance and repair response lead to PC [4]. Thus, the inflammatory process is crucial and a better understanding of the inflammatory markers defining this “injury-inflammation-cancer” pathway could aide in the identification of novel molecular targets for the treatment of PC. For example, during the inflammation process the substance P/neurokinin-1 receptor system is up-regulated and the neurokinin-1 receptor therefore is An important target for the treatment of inflammatory processes (Figure1)[5]. Cancers 2015, 7 1217 Cancers 2015, 7 3 FigureFigure 1. 1. RiskRisk factors factors (tobacco smoking,smoking, alcoholism,alcoholism, depression)depression) for for the the development development of of PC PCare are characterized characterized by An by up-regulation an up-regulation of the SP/NK-1 of the receptorSP/NK system.-1 receptor This up-regulationsystem. This is upalso-regulation present inis inflammationalso present andin inflammation in chronic pancreatitis. and in chroni Smokingc pancreatitis. and alcohol Smoking abuse induce and alcohola pro-inflammatory abuse induce milieu a pro and-inflammatory are risk factors milieu for chronic and pancreatitis;are risk factors depression for increaseschronic pancreatitis;the level of SP,depression and chronic increases pancreatitis the level promotes of SP, PC. and NK-1 chronic receptor pancreatitis antagonists promotes can prevent PC. NK(by-1 counteractingreceptor antagonists the risk factors/chroniccan prevent pancreatitis)(by counteracting and can th treate risk PC factors/chronic by blocking the pancreatitis)pathophysiological and can actionstreat PC exerted by blocking by SP the via pathophysiological the NK-1 receptor. actions exerted by SP via the NK-1 receptor. It is known that the risk factor of PC is 13.6% for tobacco smoking and 13.0% for heavy alcohol drinking,It is known and that that the the risk risk factor of PC of increases PC is 13.6% to 25.7% for tobacco when considering smoking and tobacco 13.0% smoking for heavy and alcohol alcohol drinking,together and [6]. that This the means risk of that PC An increases appreciable to 25.7% proportion when considering of the PC population tobacco smoking could be and avoided alcohol by togethermodifying [6]. lifestyle This means habits that such an as tobaccoappreciable smoking proportion and heavy of the alcohol PC population drinking. Smoking could be and avoided alcoholism by modifyingare well-established lifestyle habits risk factors such of as chronic tobacco pancreatitis smoking and and PC heavy [6] and alcohol chronic drinking. pancreatitis Smoking is a risk factorand alcoholismfor the development are well-established of PC [7] risk (Figure factors1). Moreover,of chronic itpancreatitis has been reportedand PC [ that6] and chronic chronic stress pancreatitis increases issusceptibility a risk factor forfor developingthe development pancreatitis of PC and [7] accelerates(Figure 1). PCMoreover growth, andit has invasion been reported [8,9]. that chronic stressPeptides increases are susceptibility widely involved for developi in humanng pathology pancreatitis (see and [5 ]accelerates for a review). PC growth As indicated and invasion above, [ one8,9] of. thesePeptides peptides are widely is the undecapeptide involved in human substance pathology P (SP). (see The [5 biological] for a review action). As of SPindicated is mainly above, mediated one of by thesethe tachykininpeptides is neurokinin-1 the undecapeptide receptor substance (NK-1 receptor), P (SP). The since biological SP shows action the highest of SP affinityis mainly for med theiated NK-1 byreceptor the tachykinin [10]. Many neurokinin data indicate-1 receptor that the (NK SP/NK-1-1 receptor), receptor since system SP shows is involved the highest in smoking, affinity alcoholism, for the NKdepression,-1 receptor chronic [10]. inflammationMany data indicate and cancer that progressionthe SP/NK-1 (Figure receptor1)[ 5system,11,12 ].is Thisinvolved is very in important,smoking, alcoholism,since it means depression that a therapeutic, chronic inflammation intervention with and NK-1cancer receptor progression antagonists (Figure by 1) targeting [5,11,12] NK-1. This receptors is very important,could improve since theit means above pathologiesthat a therapeutic (Figure i1ntervention). This strategy with opensNK-1 up receptor new approaches antagonists for by translational targeting NKresearch.-1 receptors In view could of this, improve the aim the of above this paper pathologies is to review (Figure the involvement 1). This strategy of the SP/NK-1opens up receptor new system in these pathologies and, in particular, in PC. Cancers 2015, 7 1218 2. Substance P and the
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