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α5-nAChR modulates nicotine-induced cell migration and invasion in A549 lung cancer cells.
Abstract Cigarette smoking is the most important risk factor in the development of human lung cancer. Nicotine, the major component in tobacco, not only contributes to carcinogenesis but also promotes tumor metastasis. By binding to nicotinic acetylcholine receptors (nAChRs), nicotine induces the proliferation and migration of non-small cell lung cancer. Recently studies have indicated that α5-nAChR is highly associated with lung cancer risk and nicotine dependence. Nevertheless, it is unclear whether nicotine promotes the migration and invasion through activation of α5-nAChR in lung cancer. In the present study...
Source: Experimental and Toxicologic Pathology - July 20, 2015 Category: Pathology Authors: Sun H, Ma X Tags: Exp Toxicol Pathol Source Type: research

Abstract 4456: Aurora-A is a downstream target of RAS and forms a positive feedback regulation loop with NF-{kappa}B in non-small cell lung cancer
Previous studies have shown that inhibition of Aurora-A reduces mutant RAS oncogenic activity and that both Aurora-A and RAS activate NF-κB pathway through phosphorylation of IkBa and upregulation of GSKa, respectively. Here we show that Aurora-A expression and kinase activity are regulated by activating mutation of KRAS. Blockage of NF-κB by IκB-S32/36A abrogated KRAS-induced Aurora-A expression and kinase activity. Furthermore, we demonstrated that NF-κB directly bound to Aurora-A promoter and induces Aurora-A transcription. In addition, depletion of Aurora-A by siRNA and pharmacological inhibitor MLN8237 suppresses ...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Kim, D., Kanai, M., Zheng, X., Zheng, D., Coppola, D., Cheng, J. Q. Tags: Molecular and Cellular Biology Source Type: research

Nicotine-mediated invasion and migration of non-small cell lung carcinoma cells by modulating STMN3 and GSPT1 genes in an ID1-dependent manner
Conclusions: Collectively, our data suggests that nicotine and EGF induce genes such as STMN3 and GSPT1 to promote the proliferation, invasion and migration of NSCLC, thus enhancing their tumorigenic properties. These studies thus reveal a central role for ID1 and its downstream targets in facilitating lung cancer progression.
Source: Molecular Cancer - July 16, 2014 Category: Cancer & Oncology Authors: Sajitha NairNamrata Bora-SinghalDeepak PerumalSrikumar Chellappan Source Type: research

Alpha5 nicotinic acetylcholine receptor mediates nicotine-induced HIF-1α and VEGF expression in non-small cell lung cancer.
Abstract By binding to nicotinic acetylcholine receptors (nAChRs), nicotine induces the proliferation and apoptosis of non-small cell lung cancer (NSCLC). Previous studies have indicated that α5-nAChR is highly associated with lung cancer risk and nicotine dependence. However, the mechanisms through which α5-nAChRs may influence lung carcinogenesis are far from clear. In the present study, we investigated the roles of α5-nAChR in the nicotine-induced expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF). Immunohistochemistry was used to detect the expression of α5-n...
Source: Toxicology and Applied Pharmacology - April 30, 2014 Category: Toxicology Authors: Ma X, Jia Y, Zu S, Li R, Jia Y, Zhao Y, Xiao D, Dang N, Wang Y Tags: Toxicol Appl Pharmacol Source Type: research

GW1929 inhibits α7 nAChR expression through PPARγ-independent activation of p38 MAPK and inactivation of PI3-K/mTOR: The role of Egr-1.
Abstract Studies demonstrated that peroxisome proliferator-activated receptor gamma (PPARγ) ligands reduce nicotine-induced non small cell lung carcinoma (NSCLC) cell growth through inhibition of nicotinic acetylcholine receptor (nAChR) mediated signaling pathways. However, the mechanisms by which PPARγ ligands inhibited nAChR expression remain elucidated. Here, we show that GW1929, a synthetic PPARγ ligand, not only inhibited but also antagonized the stimulatory effect of acetylcholine on NSCLC cell proliferation. Interestingly, GW1929 inhibited α7 nAChR expression, which was not blocked by GW9662, an antagon...
Source: Cellular Signalling - January 8, 2014 Category: Cytology Authors: Hahn SS, Tang Q, Zheng F, Zhao S, Wu J Tags: Cell Signal Source Type: research