A Small Cell Lung Carcinoma Line and Subclone Expressing Nicotinic Acetylcholine Receptors of Muscle and Neuronal Types<sup>a</sup>

Sciamanna, Michele A.; Griesmann, Guy E.; Lennon, Vanda A.

doi:10.1111/j.1749-6632.1998.tb10998.x

Cited by 2 publications

(4 citation statements)

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“…This nicotinic receptor accessory protein, described by Miwa et al [138] and Ibanez-Tallon et al [139], appears to modulate responses to ACh by α7 and α4β2 nAChRs and to enhance receptor desensitization by nicotine. Because bronchial epithelium is exposed to some of the highest levels of nicotine in the body, it is likely that lynx1 will play a key role in modulating the effect of nicotine on autocrine cholinergic [3,5,6,13,159,[162][163][164][165][166][167][168][169][170] Fetal pulmonary neuroendocrine cells [169][170][171] Normal human bronchial epithelial cells [10,12,143,[171][172][173] Small airway epithelial cells [143,171] Lung & mesothelial & mesothelioma [14,[174][175] Human embryonic pulmonary fibroblast cell line [176] Fig . (10).…”

Section: Non-neuronal Nicotinic Ach Receptor (Nachr) In Lung and Pleumentioning

confidence: 99%

Development of Novel Therapeutic Strategies for Lung Cancer: Targeting the Cholinergic System

Russo¹,

Catassi²,

Cesario³

et al. 2006

CMC

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One of the earliest descriptions of non-neuronal ACh synthesis was by Morris who reported that ACh was synthesized in the placenta [1]; furthermore, Falugi et al. showed the presence of AChE in human fibrosarcoma cells [2]. Afterward, the expression of ACh, AChE, and cholinergic receptors in non-neuronal cells was reported in several studies [3-16]. Indeed, recent data reported that SCLC expresses a cholinergic autocrine loop that can regulate cell growth. Such work demonstrates that SCLC cells have a cholinergic phenotype and that ACh exerts as an autocrine growth factor in human lung tumours [16]. Moreover, it has been recently reported that nicotine in lung adenocarcinoma A549 cells, potently induces Bad phosphorylation at serine (S)112, S136 and S155 in a mechanism involving activation of MAPKs, ERK1/2, PI3K/AKT and PKA through the linking to alpha7-receptors [9]. Bad phosphorylation results in sequestering Bad from mitochondria and subsequently interacting with 14-3-3 in the cytosol [9]. We have recently reported that human malignant pleural mesothelioma expresses a cholinergic system, involved in cell growth regulation. Hence, mesothelioma cells growth is modulated by the cholinergic system in which agonists (i.e. nicotine) have a proliferative effect and antagonists (i.e. curare or alpha-cobratoxin) have an inhibitory effect. Furthermore apoptosis mechanisms are under the control of the cholinergic system (nicotine antiapoptotic via induction of NF-kappaB complexes and phosphorylation of Bad at S112, curare proapoptotic via G0-G1 arrest p21waf-1-dependent, but p53-independent) [16]. The involvement of the non-neuronal cholinergic system in lung cancer and mesothelioma appears reasonable and opens up new translational research strategies.

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Section: Non-neuronal Nicotinic Ach Receptor (Nachr) In Lung and Pleumentioning

confidence: 99%

Development of Novel Therapeutic Strategies for Lung Cancer: Targeting the Cholinergic System

Russo¹,

Catassi²,

Cesario³

et al. 2006

CMC

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“…SCLC Lines. SCC37 was established from the lymph node metastasis of a 72-year-old woman with clinically and serologically evident MG. 7,8 A control cell line, SCC81, was established from the lymph node metastasis of a 56-year-old woman who was seropositive for antineuronal nuclear autoantibody type 1 (ANNA1/ anti-Hu) with sensory neuronopathy. Cells were cultured in Roswell Park Memorial Institute (RPMI) media supplemented with 10% bovine calf serum, penicillin, streptomycin, and glutamine.…”

Section: Methodsmentioning

confidence: 99%

“…SCC37 was established from the lymph node metastasis of a 72‐year‐old woman with clinically and serologically evident MG . A control cell line, SCC81, was established from the lymph node metastasis of a 56‐year‐old woman who was seropositive for antineuronal nuclear autoantibody type 1 (ANNA1/ anti‐Hu) with sensory neuronopathy.…”

Section: Methodsmentioning

confidence: 99%

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A Small Cell Lung Carcinoma Line and Subclone Expressing Nicotinic Acetylcholine Receptors of Muscle and Neuronal Types^a

Cited by 2 publications

References 11 publications

Development of Novel Therapeutic Strategies for Lung Cancer: Targeting the Cholinergic System

Development of Novel Therapeutic Strategies for Lung Cancer: Targeting the Cholinergic System

Mutated cancer autoantigen implicated cause of paraneoplastic myasthenia gravis

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A Small Cell Lung Carcinoma Line and Subclone Expressing Nicotinic Acetylcholine Receptors of Muscle and Neuronal Typesa

Cited by 2 publications

References 11 publications

Development of Novel Therapeutic Strategies for Lung Cancer: Targeting the Cholinergic System

Development of Novel Therapeutic Strategies for Lung Cancer: Targeting the Cholinergic System

Mutated cancer autoantigen implicated cause of paraneoplastic myasthenia gravis

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A Small Cell Lung Carcinoma Line and Subclone Expressing Nicotinic Acetylcholine Receptors of Muscle and Neuronal Types^a