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Beta arrestin1 associated genomic regions in nicotine induced Non-Small Cell Lung Carcinoma (NSCLC) cell line A549

ABSTRACT: The multifunctional scaffolding protein M-NM-2-arrestin-1 plays a vital role in mediating the proliferative effects of nicotine through nAChR signaling. M-NM-2-arrestins were initially known as negative regulators of GPCR mediated signaling as they promote internalization and desensitization of GPCRs. However, new roles of M-NM-2-arrestins in receptor trafficking and signaling have been discovered in recent years. They are known to regulate signaling through a number of receptors such as Notch, endothelin A receptor, frizzled, smoothened and the nicotinic cholinergic receptors. Studies from our lab revealed that nAChR signaling induces the translocation of M-NM-2-arrestin-1 to the nucleus, in a Src dependent manner, where it directly binds to the proliferative E2Fs. Furthermore, the nuclear translocation of M-NM-2-arrestin-1 results in recruitment of p300 to E2F1 regulated proliferative promoters facilitating histone acetylation and transcription of these promoters. Given the role of M-NM-2-arrestin-1 in nicotine induced gene expression, we attempted to explore the global association of M-NM-2-arrestin-1 to the genomic regions upon nicotine stimulation by ChIP sequencing. It was found that M-NM-2-arrestin-1 is recruited on the promoters of many genes that regulate EMT as well as other regulatory pathways. In this assay, M-NM-2-arrestin-1 was found to be associated with the promoter regions of genes such as ZNF768, ZNF131, CSF3R, HMGA2, TAL1, RCC1, NKX2-4 etc in response to nicotine stimulation. Serum starved/quiescent A549 cells and Nicotine stimulated A549 cells

ORGANISM(S): Homo sapiens

SUBMITTER: Jonathan Nguyen

PROVIDER: E-GEOD-40689 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Beta arrestin1 associated genomic regions in nicotine induced Non-Small Cell Lung Carcinoma (NSCLC) cell line A549

Project description:The multifunctional scaffolding protein β-arrestin-1 plays a vital role in mediating the proliferative effects of nicotine through nAChR signaling. β-arrestins were initially known as negative regulators of GPCR mediated signaling as they promote internalization and desensitization of GPCRs. However, new roles of β-arrestins in receptor trafficking and signaling have been discovered in recent years. They are known to regulate signaling through a number of receptors such as Notch, endothelin A receptor, frizzled, smoothened and the nicotinic cholinergic receptors. Studies from our lab revealed that nAChR signaling induces the translocation of β-arrestin-1 to the nucleus, in a Src dependent manner, where it directly binds to the proliferative E2Fs. Furthermore, the nuclear translocation of β-arrestin-1 results in recruitment of p300 to E2F1 regulated proliferative promoters facilitating histone acetylation and transcription of these promoters. Given the role of β-arrestin-1 in nicotine induced gene expression, we attempted to explore the global association of β-arrestin-1 to the genomic regions upon nicotine stimulation by ChIP sequencing. It was found that β-arrestin-1 is recruited on the promoters of many genes that regulate EMT as well as other regulatory pathways. In this assay, β-arrestin-1 was found to be associated with the promoter regions of genes such as ZNF768, ZNF131, CSF3R, HMGA2, TAL1, RCC1, NKX2-4 etc in response to nicotine stimulation.

2013-12-16 | GSE40689 | GEO

Nicotinic acetylcholine receptors and EGF induce c-Kit ligand/Stem Cell Factor (SCF) in a M-NM-2-arrestin-1 and E2F1 dependent manner in NSCLC

Project description:Lung cancer remains the leading cause of cancer-related deaths worldwide. M-NM-2-arrestin-1 (ARRB1), a scaffolding protein involved in the termination or desensitization of signals arising from activated G-protein-coupled receptors (GPCRs) has been shown to play a role in invasion and proliferation of many cancers, including nicotine-induced proliferation of human nonM-bM-^@M-^Ssmall cell lung cancers (NSCLCs). In this study, we analyzed nicotine induced and M-NM-2-arrestin-1 dependent genes from the microarray data. Our analysis show that SCF (Stem cell factor) strongly differentiated smokers from non-smokers implying an important role of this gene in NSCLCs. SCF, a major cytokine is the ligand for the c-Kit proto-oncogene. Here we elucidate the molecular mechanisms by which nicotine as well as EGF induces the expression of SCF in lung adenocarcinoma cell lines A549 and H1650. ChIP assays and transient transfection experiments showed that transcription factor E2F1 can positively regulate SCF expression at the transcriptional level; depletion of E2F1 or M-NM-2-arrestin-1 prevented the nicotine-mediated induction of SCF. Given that the binding of SCF to c-Kit leads to activation of multiple downstream signaling pathways including Src, PI3K, MEK and EGFR pathways, our data suggest that the SCF plays a central role in lung carcinogenesis, and may be a potential therapeutic target for combating NSCLC. Studies presented here also provide evidence that SCF along with nicotine promotes self-renewal and proliferation of lung cancer stem cells (CSCs). Our findings reveal an important role and prognostic significance of SCF that can serve as a novel prognostic and predictive biomarker for NSCLC. Transfection of A549 cell line with control siRNA, Beta arrestin siRNA and then stimulation of nicotine

2013-11-10 | E-GEOD-44617 | biostudies-arrayexpress

Expression data from CHRNA5 knockdown A549 lung cancer cells compared with control

Project description:Nicotine and nicotinic acetylcholine receptors (nAChRs) are considred to be involved in the progression of lung carcinomas. α5-nAChR is believed to be associated with lung cancer risk and onset, however its function and physiologic roles is far from clear. We use microarry to detail the global programme of gene expression underlying knockdown CHRNA5, encoding α5-nAChR, in human lung cancer A549 cells compared with control.

2017-09-20 | GSE101979 | GEO

Transcription profiling of human model neuronal cell lines after chronic nicotine exposure

Project description:The long-term goal of this project is to establish whether and how chronic nicotine exposure affects nervous system function. The biological targets of nicotine action are diverse members of the superfamily of neurotransmitter-gated ion channels called nicotinic acetylcholine receptors (nAChR). nAChR play multiple, critical roles in chemical signaling throughout the brain and body. They also must be involved in nicotine dependence, which drives tobacco product use responsible for tremendous economic and personal costs. To define changes in gene expression induced by nicotine exposure in a model neuronal cell lines expressing at least two nicotinic receptor subtypes. Nicotine exposure exerst at least some of its effects on nervous system function by altering gene expression. Cells of the SH-SY5Y human neuroblastoma will be exposed to an efficacious dose of nicotine or to control medium for two different periods.

2008-06-11 | E-GEOD-11208 | biostudies-arrayexpress

Chronic nicotine exposure (kuo-affy-human-232930)

2008-04-19 | GSE11208 | GEO

Mammary tumors of xenograft mice with the treatment of nicotine and JMY117 as well as CHRNA9 and SLC19A7 knockdown in MDA-MB-231, A549 and Hep3B cells

Project description:First, we want to know whether JMY117 (Bupropion) would act as a blockade to attenuate nicotine induced cancer metastatic effect. With two months observations, we discovered that nicotine treatment (10 µg/ml) via drinking water significantly increased tumor distant metastasis. Furthermore, using 100 and 200 µg/kg JMY117 three times per week significantly suppressed the numbers of lung metastasis nodules on both with or without nicotine treatment, indicating JMY117 not only block the signals from nicotine but also inhibits the signals from other endogenous nAChR agonists. In addition, we also investigated the roles of CHRNA9 and SLC16A7 in breast cancer (MDA-MB-231), lung cancer (A549) and liver cancer (Hep3B) cell lines

2018-02-10 | GSE105445 | GEO

Alpha7 Nicotinic Acetylcholine Receptor Mediates Chronic Nicotine Inhalation-Induced Cardiopulmonary Dysfunction

Project description:Purpose: The goal of this study is to compare the effects of inhaled nicotine on aortic gene expression and the role of the alpha7 nicotinic acetylcholine receptor (alpha7-nAChR) in mediating the nicotine effects. Methods: WT and alpha7-nAChR knockout (KO) mice at 5-month of age were exposed to nicotine vapor or room air for a total of 12 weeks. Total RNA was extracted from thoracic aortas using RNeasy Plus mini kit followed by library preparation using SMART-Seq v4 Ultra Low Input RNA Kit. Illumina next generation sequencing was performed using the NextSeq 500 system with the high output flow cell (up to 800 M paired end reads). Results: A total of 179 differentially expressed genes (149 upregulated and 30 downregulated, adjusted P-value < 0.1) were found in thoracic aortas from WT mice exposed to nicotine vapor compared to those exposed to room air. In contrast, only 7 non-overlapping genes were found to be differentially expressed in alpha7-nAChR KO mice exposed to nicotine compared to the air controls. Conclusions: Our study suggests that nicotine-induced changes in vascular gene expression is largely mediated by the alpha7-nAChR.

2022-02-08 | GSE196184 | GEO

Nicotine effect on CEM model T cell line (kuo-affy-human-232861)

Project description:The long-term objective of this project is to establish roles played in development and function of the immune system by nicotinic acetylcholine receptors (nAChR) and exposure to the tobacco alkaloid, nicotine. The planned gene chip studies will allow us to assess effects of nicotine exposure on gene expression in a model T cell line, and the findings are expected to help direct further efforts. One of the biomedically-relevant hypotheses of this project is that tobacco use and nicotine exposure affect immune system development. To establish effects of nicotine exposure on gene expression in the CEM model T cell line. Immune system nAChR acting as ion channels or via novel signaling cascades mediate their effects on T cell development by altering expression of genes involved in T cell receptor rearrangements, cytokine expression, and cell death/survival decisions. CEM cells will be treated for one hour or one day with an effective dose of nicotine or with the same medium change but in the absence of nicotine. Keywords: nicotine, T cell line

2008-04-11 | E-GEOD-11142 | biostudies-arrayexpress

Nicotine effect on CEM model T cell line (kuo-affy-human-232861)

2008-04-12 | GSE11142 | GEO

Downstream targets of ID1 transcription factor in Non-Small Cell Lung Carcinoma (NSCLC)

Project description:ID-1, known as inhibitor of differentiation or a helix loop helix transcription factor which lack the basic DNA binding domain. It is known to bind to bHLH transcription factor and inhibit those bHLH to bind to the promoter thus inhibiting further transcription. Overexpression of ID-1 has been correlated with a variety of human cancers including breast, prostate, pancreatic, ovarian, endometrial, bladder cancer and melanomas. Recently known that if ID-1 is depleted, it abrogates cell proliferation, invasion and migration of cells in NSCLC. Further ID-1 expression is induced by Nicotine and EGF through the activation of nAChRs and EGFR. Here microarray analysis was done to compare differential gene expression patterns upon nicotine and EGF stimulation of A549 and H1650 cells and how ID1 depletion changes these patterns. We find that multiple genes are affected and the role of these genes in lung cancer will be elucidated. In this study we show that ID-1 regulates the expression of three genes STMN3, TPD52 and GSPT1 in NSCLC by activating the promoter of these genes either directly or indirectly. We also show that depletion of STMN3, TPD52 and GSPT1 prevented Nicotine and EGF induced cell proliferation, invasion and migration of cells in NSCLC. Two cell lines (A549, H1650) each having 5 samples.

2013-04-15 | E-GEOD-38944 | biostudies-arrayexpress

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