A new twist to neurotransmitter receptors and cancer

Schüller, Hildegard M.

doi:10.20517/2394-4722.2017.18

Cited by 10 publications

(13 citation statements)

References 69 publications

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“…Nicotine’s effect likely involves the epidermal growth factor receptors (EGFRs), since it has been previously reported that nicotine induces secretion of growth factors leading to tumor progression and metastasis [ 7 ]. Binding of nicotine to α7nAChRs can induce the secretion of growth factors, such as EGF, IGF, along with neurotransmitters, such as adrenaline and noradrenaline [ 7 , 48 ]. This nicotine-mediated increased secretion of EGF and IGF leads to the transactivation of EGFR and IGF-1R, resulting in the activation of mitogenic and antiapoptotic pathways [ 7 , 48 ].…”

Section: Resultsmentioning

confidence: 99%

“…Binding of nicotine to α7nAChRs can induce the secretion of growth factors, such as EGF, IGF, along with neurotransmitters, such as adrenaline and noradrenaline [ 7 , 48 ]. This nicotine-mediated increased secretion of EGF and IGF leads to the transactivation of EGFR and IGF-1R, resulting in the activation of mitogenic and antiapoptotic pathways [ 7 , 48 ]. Moreover, release of adrenaline and noradrenaline, the physiological ligands for β-AR, upon binding of nicotine to α7nAChRs, activates the β-AR which, in turn, stimulates release of EGF and IGF, thereby promoting growth and proliferation contributing to lung cancer progression [ 7 , 48 ].…”

Section: Resultsmentioning

confidence: 99%

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Regulation of Cisplatin Resistance in Lung Cancer Cells by Nicotine, BDNF, and a β-Adrenergic Receptor Blocker

Ray

Khashali

Haddad

et al. 2022

IJMS

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It is well-recognized that cigarette smoking is a primary risk factor in the development of non-small cell lung cancer (NSCLC), known to account for ~80% of all lung cancers with nicotine recognized as the major addictive component. In investigating the effect of nicotine, brain-derived neurotrophic factor (BDNF), and the β-adrenergic receptor blocker, propranolol, on sensitivity of NSCLC cell lines, A549 and H1299, to cisplatin, we found increased cell viability, and enhanced cisplatin resistance with nicotine and/or BDNF treatment while opposite effects were found upon treatment with propranolol. Cell treatment with epinephrine or nicotine led to EGFR and IGF-1R activation, effects opposite to those found with propranolol. Blocking EGFR and IGF-1R activation increased cell sensitivity to cisplatin in both cell lines. PI3K and AKT activities were upregulated by nicotine or BDNF and downregulated by cell treatment with inhibitors against EGFR and IGF-1R and by propranolol. Apoptosis and cell sensitivity to cisplatin increased upon co-treatment of cells with cisplatin and inhibitors against PI3K or AKT. Our findings shed light on an interplay between nicotine, BDNF, and β-Adrenergic receptor signaling in regulating survival of lung cancer cells and chemoresistance which can likely expand therapeutic opportunities that target this regulatory network in the future.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Regulation of Cisplatin Resistance in Lung Cancer Cells by Nicotine, BDNF, and a β-Adrenergic Receptor Blocker

Ray

Khashali

Haddad

et al. 2022

IJMS

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“…Pulmonary neuroepithelial bodies (NEB) are innervated serotonin (5-HT)-producing cells distributed throughout the airway epithelium. Studies have reported that 5-HT secretion can stimulate cancer progression, including cancer proliferation, migration, and invasion [ 20 , 21 ]. The data in Figure 1 provide evidence that AZ, SFN, and their combination show dose-dependent reduction in scratch wound closure by the bronchial carcinoid H727 (typical carcinoid) cells.…”

Section: Resultsmentioning

confidence: 99%

Next-generation multimodality of nutrigenomic cancer therapy: sulforaphane in combination with acetazolamide actively target bronchial carcinoid cancer in disabling the PI3K/Akt/mTOR survival pathway and inducing apoptosis

et al. 2021

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Objective: Aberrations in the PI3K/AKT/mTOR survival pathway in many cancers are the most common genomic abnormalities. The phytochemical and bioactive agent sulforaphane (SFN) has nutrigenomic potential in activating the expression of several cellular protective genes via the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2). Nrf2 is primarily related to mechanisms of endogenous cellular defense and survival. The efficacy of SFN in combination with acetazolamide (AZ) was investigated in reducing typical H727 and atypical H720 BC survival, migration potential, and apoptosis in vitro and in vivo preclinical xenograft tissues. Materials and Methods: Microscopic imaging, immunocytochemistry, wound healing assay, caspase-cleaved cytokeratin 18 (M30, CCK18) CytoDeath ELISA assay, immunofluorescence labeling assays for apoptosis, hypoxia, Western Blotting, Tunnel assay, measurement of 5-HT secretion by carbon fiber amperometry assay, quantitative methylation-specific PCR (qMSP), morphologic changes, cell viability, apoptosis activity and the expression levels of phospho-Akt1, Akt1, HIF-1α, PI3K, p21, CAIX, 5-HT, phospho-mTOR, and mTOR in xenografts derived from typical H727 and atypical H720 BC cell lines. Results: Combining AZ+SFN reduced tumor cell survival compared to each agent alone, both in vitro and in vivo xenograft tissues. AZ+SFN targeted multiple pathways

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“…Neurotransmitter signaling can modulate different aspects of cancer development, such as proliferation, invasion, metastasis [221,222,223,224]. (See BOX 2 for autonomic pancreatic innervation [225,226]).…”

Section: Molecules and Pathways Involved In Pnimentioning

confidence: 99%

Nerves and Pancreatic Cancer: New Insights into A Dangerous Relationship

Gasparini

Pellegatta

Crippa

et al. 2019

Cancers

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Perineural invasion (PNI) is defined as the presence of neoplastic cells along nerves and/or within the different layers of nervous fibers: epineural, perineural and endoneural spaces. In pancreatic cancer—particularly in pancreatic ductal adenocarcinoma (PDAC)—PNI has a prevalence between 70 and 100%, surpassing any other solid tumor. PNI has been detected in the early stages of pancreatic cancer and has been associated with pain, increased tumor recurrence and diminished overall survival. Such an early, invasive and recurrent phenomenon is probably crucial for tumor growth and metastasis. PNI is a still not a uniformly characterized event; usually it is described only dichotomously (“present” or “absent”). Recently, a more detailed scoring system for PNI has been proposed, though not specific for pancreatic cancer. Previous studies have implicated several molecules and pathways in PNI, among which are secreted neurotrophins, chemokines and inflammatory cells. However, the mechanisms underlying PNI are poorly understood and several aspects are actively being investigated. In this review, we will discuss the main molecules and signaling pathways implicated in PNI and their roles in the PDAC.

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A new twist to neurotransmitter receptors and cancer

Cited by 10 publications

References 69 publications

Regulation of Cisplatin Resistance in Lung Cancer Cells by Nicotine, BDNF, and a β-Adrenergic Receptor Blocker

Regulation of Cisplatin Resistance in Lung Cancer Cells by Nicotine, BDNF, and a β-Adrenergic Receptor Blocker

Next-generation multimodality of nutrigenomic cancer therapy: sulforaphane in combination with acetazolamide actively target bronchial carcinoid cancer in disabling the PI3K/Akt/mTOR survival pathway and inducing apoptosis

Nerves and Pancreatic Cancer: New Insights into A Dangerous Relationship

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