<i>Retracted</i>: Role of α7‐nicotinic acetylcholine receptor in human non‐small cell lung cancer proliferation

Paleari, Laura; Catassi, Alessia; Ciarlo, Monica; Cavalieri, Zita; Bruzzo, Cristina; Servent, Denis; Cesario, Alfredo; Chessa, Leonardo; Cilli, Michele; Piccardi, Federica; Granone, Pierluigi; Russo, Patrizia

doi:10.1111/j.1365-2184.2008.00566.x

Cited by 78 publications

(66 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…While all classes of nAChRs are capable of desensitization through chronic agonist exposure, there are definite immediate effects of nicotine on nAChRs in a subunitdependent manner. Although it is currently unknown whether chronic exposure of nAChR to nicotine via E-Cigs can cause lung cancer, the role of nAChR ␣7 in contributing to nonsmall cell lung cancer by altering cell proliferation and apoptotic resistance has been reported (86,113).…”

Section: Will Nicotine and Chemical Constituents In E-liquids/e-cigs mentioning

confidence: 99%

Will chronic e-cigarette use cause lung disease?

Rowell

Tarran

2015

American Journal of Physiology-Lung Cellular and Molecular Phys

103

View full text Add to dashboard Cite

Chronic tobacco smoking is a major cause of preventable morbidity and mortality worldwide. In the lung, tobacco smoking increases the risk of lung cancer, and also causes chronic obstructive pulmonary disease (COPD), which encompasses both emphysema and chronic bronchitis. E-cigarettes (E-Cigs), or electronic nicotine delivery systems, were developed over a decade ago and are designed to deliver nicotine without combusting tobacco. Although tobacco smoking has declined since the 1950s, E-Cig usage has increased, attracting both former tobacco smokers and never smokers. E-Cig liquids (e-liquids) contain nicotine in a glycerol/propylene glycol vehicle with flavorings, which are vaporized and inhaled. To date, neither E-Cig devices, nor e-liquids, are regulated by the Food and Drug Administration (FDA). The FDA has proposed a deeming rule, which aims to initiate legislation to regulate E-Cigs, but the timeline to take effect is uncertain. Proponents of E-Cigs say that they are safe and should not be regulated. Opposition is varied, with some opponents proposing that E-Cig usage will introduce a new generation to nicotine addiction, reversing the decline seen with tobacco smoking, or that E-Cigs generally may not be safe and will trigger diseases like tobacco. In this review, we shall discuss what is known about the effects of E-Cigs on the mammalian lung and isolated lung cells in vitro. We hope that collating this data will help illustrate gaps in the knowledge of this burgeoning field, directing researchers toward answering whether or not E-Cigs are capable of causing disease.

show abstract

Section: Will Nicotine and Chemical Constituents In E-liquids/e-cigs mentioning

confidence: 99%

Will chronic e-cigarette use cause lung disease?

Rowell

Tarran

2015

American Journal of Physiology-Lung Cellular and Molecular Phys

103

View full text Add to dashboard Cite

show abstract

“…Multiple studies have shown that activation of nAChRs by nicotine, which is an exogenous ligand for nAChRs, stimulates tumor cells growth in breast, 17 lung, 18 colon, 19 bladder 20 and cervical cancer. 21 The muscarinic receptors (mAChRs) are G-protein-coupled receptors, and 5 subtypes of mAChRs (M1-M5) have been identified.…”

Section: Introductionmentioning

confidence: 99%

Blocking M2 muscarinic receptor signaling inhibits tumor growth and reverses epithelial-mesenchymal transition (EMT) in non-small cell lung cancer (NSCLC)

Zhao

Zhang

et al. 2015

Cancer Biology & Therapy

View full text Add to dashboard Cite

These authors contributed equally to this work.Keywords: autoparacrine, AKT, epithelial-mesenchymal transition, MAPK ERK, M2 muscarinic receptor, non-neuronal acetylcholine, non-small cell lung cancerAbbreviations: NSCLC, non-small cell lung cancer; SCLC, small cell lung cancer; ACh, acetylcholine; AChR, acetylcholine receptor; mAChR, muscarinic receptor; nAChR, nicotinic receptor; M2R, M2 mAChR; EMT, epithelial-mesenchymal transition; ChAT, choline acetyltransferase; MAPK, mitogen-activated protein kinase; shRNA, short hairpin RNA.Lung cancers express non-neuronal, cholinergic autoparacrine loop, which facilitates tumor growth. Interruption of M3 muscarinic cholinergic signaling has been reported to inhibit small cell lung cancer (SCLC) growth. The purpose of this study is to investigate if blocking autoparacrine muscarinic cholinergic signaling could inhibit non-small cell lung cancer (NSCLC) growth and possible underlying mechanisms. Our results showed that PC9 and A549 cells expressed all 5 subtypes of muscarinic receptor (mAChR) and blocking M2 mAChR (M2R) signaling using selective antagonist methoctramine or short hairpin RNA (shRNA) inhibited tumor cell proliferation in vitro and in vivo. Consistent with AChR agonists stimulating p44/42 MAPK (Erk1/2) and Akt phosphorylation, blocking M2R signaling decreased MAPK and Akt phosphorylation, indicating that non-neuronal ACh functions as an autoparacrine growth factor signaling in part through activation of M2R and downstream MAPK and Akt pathways. Importantly, further studies revealed that blocking M2R signaling also reversed epithelial-mesenchymal transition (EMT) in vitro and in vivo, indicating that nonneuronal ACh promotes EMT partially through activation of M2R. These findings demonstrate that M2R plays a role in the growth and progression of NSCLC and suggest M2R antagonists may be an efficacious adjuvant therapy for NSCLC.

show abstract

“…While nAChRs are mainly expressed in neurons and neuromuscular junctions, they are also present on a variety of nonneuronal cells, where they induce cell proliferation, invasion, and angiogenesis (16,19,20,36,53,67). While there is scant evidence that nicotine contributes to the initiation of tumors, it has been demonstrated that nicotine can promote the growth and metastasis of solid tumors in vivo (10,44), suggesting that nicotine might be promoting the progression of tumors already initiated by the tobacco-specific nitrosamines (10).…”

mentioning

confidence: 99%

ID1 Facilitates the Growth and Metastasis of Non-Small Cell Lung Cancer in Response to Nicotinic Acetylcholine Receptor and Epidermal Growth Factor Receptor Signaling

Pillai

Rizwani

et al. 2011

Molecular and Cellular Biology

View full text Add to dashboard Cite

Retracted: Role of α7‐nicotinic acetylcholine receptor in human non‐small cell lung cancer proliferation

Abstract: These results showed that alpha7-nAChR plays an important role in NSCLC cell growth and tumour progression as well as in cell death.

Cited by 78 publications

References 52 publications

Will chronic e-cigarette use cause lung disease?

Will chronic e-cigarette use cause lung disease?

Blocking M2 muscarinic receptor signaling inhibits tumor growth and reverses epithelial-mesenchymal transition (EMT) in non-small cell lung cancer (NSCLC)

ID1 Facilitates the Growth and Metastasis of Non-Small Cell Lung Cancer in Response to Nicotinic Acetylcholine Receptor and Epidermal Growth Factor Receptor Signaling

Contact Info

Product

Resources

About