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Mitochondrion. 2018 May;40:58-70. doi: 10.1016/j.mito.2017.10.002. Epub 2017 Oct 16.

Cigarette smoke induces mitochondrial metabolic reprogramming in lung cells.

Author information

1
Institute of Bioinformatics, International Tech Park, Bangalore 560 066, India; School of Biotechnology, KIIT University, Bhubaneswar, Odisha 751024, India.
2
Institute of Bioinformatics, International Tech Park, Bangalore 560 066, India; Manipal University, Madhav Nagar, Manipal 576104, India.
3
Institute of Bioinformatics, International Tech Park, Bangalore 560 066, India; Amrita School of Biotechnology, Amrita University, Kollam 690 525, India.
4
Institute of Bioinformatics, International Tech Park, Bangalore 560 066, India.
5
Department of Neuro-Virology, National Institute of Mental Health and Neurosciences, Bangalore 560029, India.
6
Institute of Bioinformatics, International Tech Park, Bangalore 560 066, India; NIMHANS-IOB Proteomics and Bioinformatics Laboratory, Neurobiology Research Centre, National Institute of Mental Health and Neurosciences, Bangalore 560029, India; YU-IOB Center for Systems Biology and Molecular Medicine, Yenepoya University, Mangalore 575018, India.
7
School of Biotechnology, KIIT University, Bhubaneswar, Odisha 751024, India.
8
Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA.
9
Institute of Bioinformatics, International Tech Park, Bangalore 560 066, India. Electronic address: harsha@ibioinformatics.org.
10
Institute of Bioinformatics, International Tech Park, Bangalore 560 066, India. Electronic address: aditi@ibioinformatics.org.

Abstract

Cellular transformation owing to cigarette smoking is due to chronic exposure and not acute. However, systematic studies to understand the molecular alterations in lung cells due to cigarette smoke are lacking. To understand these molecular alterations induced by chronic cigarette smoke exposure, we carried out tandem mass tag (TMT) based temporal proteomic profiling of lung cells exposed to cigarette smoke for upto 12months. We identified 2620 proteins in total, of which 671 proteins were differentially expressed (1.5-fold) after 12months of exposure. Prolonged exposure of lung cells to smoke for 12months revealed dysregulation of oxidative phosphorylation and overexpression of enzymes involved in TCA cycle. In addition, we also observed overexpression of enzymes involved in glutamine metabolism, fatty acid degradation and lactate synthesis. This could possibly explain the availability of alternative source of carbon to TCA cycle apart from glycolytic pyruvate. Our data indicates that chronic exposure to cigarette smoke induces mitochondrial metabolic reprogramming in cells to support growth and survival.

KEYWORDS:

Cigarette smoking; Mass spectrometry; Metabolism; NSCLC

PMID:
29042306
DOI:
10.1016/j.mito.2017.10.002

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