Inhibitions by 6‐hydroxydopamine and neostigmine singly or together of gastric carcinogenesis induced by N‐methyl‐N′‐nitro‐n‐nitrosoguanidine in wistar rats

Tatsuta, Masaharu; Baba, Miyako; Taniguchi, Haruo

doi:10.1002/ijc.2910510517

Cited by 10 publications

(7 citation statements)

References 26 publications

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“…Several studies highlight the role of the sympathetic and parasympathetic nervous systems in the development of tumors and metastases. For example, our results are in accordance with the study of Tatsuta et al [13] who showed that prolonged intraperitoneal treatment with 6-OHDA attenuated the incidence of N-methyl-N´-nitro-N-nitrosoquanidine (MNNG) induced gastric cancer in rats. Likewise, Raju et al [5] demonstrated that bilaterally sympathectomized rats develop significantly smaller, more diffuse in appearance, and less invasive tumors compared with sham operated rats.…”

Section: Discussionsupporting

confidence: 93%

Chemical sympathectomy suppresses fibrosarcoma development and improves survival of tumor-bearing rats

Lackovicova

Banovska²,

Bundzikova³

et al. 2011

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Both experimental and clinical data indicate that the sympathetic nervous system may affect the development of certain tumors. To test this, in the present study we combined in vivo and in vitro approaches to study the effect of the sympathetic nervous system on proliferation of BP6-TU2 fibrosarcoma cells. First, we investigated the effect of 6-hydroxydopamine-induced sympathectomy on tumor development and survival of tumor-bearing rats. One week after chemical sympathectomy, we injected the BP6-TU2 fibrosarcoma cells intraperitoneally into male Wistar rats. The sympathectomy significantly reduced the incidence of intraperitoneal tumors and resulted in significantly improved survival of tumor-bearing rats compared to those with intact sympathetic innervation. Using immunohistochemical methods, we found neuron-specific enolase immunopositive structures within fibrosarcoma tissue, indicating innervation of tumors. Finally, an in vitro study showed elevated proliferation of BP6-TU2 fibrosarcoma cells in response to adding norepinephrine to the culture medium. Our findings indicate that sympathetic nerves directly potentiate the proliferation of BP6-TU2 fibrosarcoma cells in rats.

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Section: Discussionsupporting

confidence: 93%

Chemical sympathectomy suppresses fibrosarcoma development and improves survival of tumor-bearing rats

Lackovicova

Banovska²,

Bundzikova³

et al. 2011

neo

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“…sympathectomy, administration of β-blockers) have shown stimulatory eff ect of sympathetic nervous system on several experimental tumors, as well. For example, chemical sympathectomy performed by 6-OHDA attenuated the incidence of N-methyl-N´-nitro-N-nitrosoquanidine (MNNG) induced gastric cancer in rats (Tatsuta et al 1992), inhibited the growth pattern of LPC-1 plasmacytoma tumors in mice (Grzanna et al 1985), and also decreased the incidence of intra-abdominal fi brosarcoma tumors in rats and prolonged their survival (Lackovicova et al 2011). Similarly, bilateral surgical sympathectomy in rats resulted in the development of significantly smaller and less invasive tongue tumors than in sham-operated animals (Raju et al 2007;Raju et al 2009).…”

Section: Discussionmentioning

confidence: 99%

Sympathectomized tumor-bearing mice survive longer but develop bigger melanomas

Horváthová

Tillinger

Padová

et al. 2016

Endocrine Regulations

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Objectives.Previously we have shown that 20 days aft er the tumor cells injection smaller melanomas have been developed in chemically sympathectomized mice in comparison with animals having intact sympathetic nervous system. However, it is known that chemical sympathectomy reduces the sympathetic neurotransmission only temporarily. In the present study, we monitored the survival of the sympathectomized mice with melanoma with an attempt to fi nd out how long the suppressing eff ect of sympathectomy on the melanoma growth may endure.Methods. Th e chemical sympathectomy was performed by intraperitoneal injection of neurotoxin 6-hydroxydopamine in male C57BL/6J mice. Seven days later, the animals were injected subcutaneously with B16-F10 melanoma cells. Th en, melanoma development, survival of the tumorbearing mice and weight of the developed tumor mass were analyzed.Results. Sympathectomy delayed the development of the palpable tumors (18th day vs.14th day) and signifi cantly prolonged the survival of the tumor-bearing mice (median 34 days vs. 29 days). However, the weight of the developed melanoma was signifi cantly increased in the sympathectomized mice in comparison with the animals having intact sympathetic nervous system.Conclusions. Th e data of the present study showed that eff ect of the chemical sympathectomy, performed before the tumor growth induction, persisted even at the time when sympathetic nerves started to regenerate that resulted in a prolonged survival of the mice with melanoma. However, comparing to our previous study, in which we have shown a reduced tumor mass in earlier stages of the tumor growth, specifi cally 20 days aft er melanoma cells injection, now we indicate that in later stages of the melanoma progression, the tumor mass was signifi cantly increased in sympathectomized animals. Th ese contra-intuitive fi ndings may indicate that interventions aff ecting the sympathetic nervous system may exert complex eff ect on the tumor progression. Based on these data we may suggest that the potential therapeutic interventions aff ecting the sympathetic signaling in the tumor tissue and its microenvironment should attenuate the sympathetic neurotransmission not only temporarily but till the complete regression of the tumor tissue.

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“…16 How ever, it should be considered that pharmacological modulation or surgical transection of the autonomic nerves during cancer, including pancreatic cancer, with agents that block β-adrenergic or cholinergic signalling is a quite an old concept, dating back to the end of 1980s. [91][92][93][94][95][96] Indeed, several studies showed the beneficial effects of administering propanolol as an unselective β-blocker with reduced pancreatic cancer incidence in hamsters with ethanol-induced pancreatitis. 97 At the cellular level, β-adrenergic receptors were shown to stimulate the proliferation and migration of human pancreatic cancer cells by cAMP-dependent signalling.…”

Section: Nerves As Modulators Of Disease Progressionmentioning

confidence: 99%

Neural plasticity in pancreatitis and pancreatic cancer

Demir

Frieß

Ceyhan

2015

Nat Rev Gastroenterol Hepatol

180

146

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Pancreatic nerves undergo prominent alterations during the evolution and progression of human chronic pancreatitis and pancreatic cancer. Intrapancreatic nerves increase in size (neural hypertrophy) and number (increased neural density). The proportion of autonomic and sensory fibres (neural remodelling) is switched, and are infiltrated by perineural inflammatory cells (pancreatic neuritis) or invaded by pancreatic cancer cells (neural invasion). These neuropathic alterations also correlate with neuropathic pain. Instead of being mere histopathological manifestations of disease progression, pancreatic neural plasticity synergizes with the enhanced excitability of sensory neurons, with Schwann cell recruitment toward cancer and with central nervous system alterations. These alterations maintain a bidirectional interaction between nerves and non-neural pancreatic cells, as demonstrated by tissue and neural damage inducing neuropathic pain, and activated neurons releasing mediators that modulate inflammation and cancer growth. Owing to the prognostic effects of pain and neural invasion in pancreatic cancer, dissecting the mechanism of pancreatic neuroplasticity holds major translational relevance. However, current in vivo models of pancreatic cancer and chronic pancreatitis contain many discrepancies from human disease that overshadow their translational value. The present Review discusses novel possibilities for mechanistically uncovering the role of the nervous system in pancreatic disease progression.

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Inhibitions by 6‐hydroxydopamine and neostigmine singly or together of gastric carcinogenesis induced by N‐methyl‐N′‐nitro‐n‐nitrosoguanidine in wistar rats

Cited by 10 publications

References 26 publications

Chemical sympathectomy suppresses fibrosarcoma development and improves survival of tumor-bearing rats

Chemical sympathectomy suppresses fibrosarcoma development and improves survival of tumor-bearing rats

Sympathectomized tumor-bearing mice survive longer but develop bigger melanomas

Neural plasticity in pancreatitis and pancreatic cancer

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