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Cigarette smoke induces angiogenic activation in the cancer field through dysregulation of an endothelial microRNA

ABSTRACT: Cigarette smoke induces angiogenic activation in the cancer field through dysregulation of an endothelial microRNA

PROVIDER: PRJNA1226536 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32426253_1.fastq.gz	Fastqsanger.gz
	SRR32426253_2.fastq.gz	Fastqsanger.gz
	SRR32426254_1.fastq.gz	Fastqsanger.gz
	SRR32426254_2.fastq.gz	Fastqsanger.gz
	SRR32426255_1.fastq.gz	Fastqsanger.gz

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Cigarette smoke induces angiogenic activation in the cancer field through dysregulation of an endothelial microRNA

Project description:Exposure to cigarette smoke induces the angiogenic activation of the endothelial cells in the cancer field by selective degradation of mature microRNA-1. This change can be detected in the lungs of non-small cell lung cancer patients and correlates with their smoking burden.

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Effect of cigarette smoke on microRNA expression in H292 lung cancer cells

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Cigarette smoke induces mitochondrial metabolic reprogramming in lung cells

Project description:Cigarette smoking remains the leading cause of non-small cell lung carcinoma. Studies involving acute exposure of smoke on lung cells revealed induction of pre- cancerous state in lung cells. Recently few studies have reported the chronic effect of cigarette smoke in inducing cellular transformation. Yet no systemic study has been performed to understand the molecular alterations in lung cells due to cigarette smoke. Hence it is both important and necessary to study the chronic effect of cigarette smoke in a temporal setting to understand the molecular alterations. In this study, we carried out TMT based proteomic profiling of lung cells which were exposed to cigarette smoke condensate (CSC) for upto 12 months. We identified 2621 proteins in total, of which 145, 114, 87, 169 and 671 proteins were differentially expressed (p<0.05, 1.5 fold) in 2nd, 4th, 6th, 8th and 12th month respectively. Pathway analysis revealed enrichment of xenobiotic metabolism signaling for the first 8 months of smoke treatment, where as continued exposure of smoke for 12 months revealed mitochondrial reprogramming in cells which includes dysregulation of oxidative phosphorylation machinery leading to enhanced reactive oxygen species and higher expression of enzymes involved in tricarboxylic acid cycle (TCA). In addition, chronic exposure of smoke led to overexpression of enzymes involved in glutamine metabolism, fatty acid degradation and lactate synthesis. This could possibly explain the availability of alternative source of carbon in TCA cycle apart from glycolytic pyruvate. Our data indicates that chronic exposure to cigarette smoke induces mitochondrial metabolic transformation in cells to support growth and survival.

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Project description:normal human bronchial epithelial cultures from two cultures in parallel exposed to cigarette smoke (CS) or air (mock) at timepoints 4 hours and 24 hours. Keywords = cigarette smoke Keywords = microarray Keywords = bronchial cell Keywords = tobacco Keywords: time-course

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mouse lung resistance or sensitivity to cigarette smoke

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