Role of Autophagy and Apoptosis in Non-Small-Cell Lung Cancer

Non-small-cell lung cancer (NSCLC) constitutes 85% of all lung cancers, and is the leading cause of cancer-related death worldwide. The poor prognosis and resistance to both radiation and chemotherapy warrant further investigation into the molecular mechanisms of NSCLC and the development of new, mo...

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Bibliographic Details
Published in:International journal of molecular sciences 2017-02, Vol.18 (2), p.367-367
Main Authors: Liu, Guangbo, Pei, Fen, Yang, Fengqing, Li, Lingxiao, Amin, Amit Dipak, Liu, Songnian, Buchan, J Ross, Cho, William C
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Apoptosis - drug effects
Apoptosis - genetics
Apoptosis Regulatory Proteins - metabolism
Autophagy
Autophagy - drug effects
Autophagy - genetics
Carcinoma, Non-Small-Cell Lung - genetics
Carcinoma, Non-Small-Cell Lung - metabolism
Carcinoma, Non-Small-Cell Lung - therapy
Cell Communication
Cellular stress response
crosstalk
endoplasmic reticulum (ER) stress
Endoplasmic Reticulum Stress - drug effects
Energy Metabolism
Genetic Variation
Humans
Immunotherapy
Lung cancer
Lung Neoplasms - genetics
Lung Neoplasms - metabolism
Lung Neoplasms - therapy
mammalian target of rapamycin (mTOR)
MAP Kinase Signaling System
Molecular Targeted Therapy
Non-small cell lung carcinoma
non-small-cell lung cancer (NSCLC)
p53
Pharmaceutical industry
Protein Binding
Review
Risk Factors
Signal Transduction
Stress, Physiological
TOR Serine-Threonine Kinases - metabolism
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Summary:Non-small-cell lung cancer (NSCLC) constitutes 85% of all lung cancers, and is the leading cause of cancer-related death worldwide. The poor prognosis and resistance to both radiation and chemotherapy warrant further investigation into the molecular mechanisms of NSCLC and the development of new, more efficacious therapeutics. The processes of autophagy and apoptosis, which induce degradation of proteins and organelles or cell death upon cellular stress, are crucial in the pathophysiology of NSCLC. The close interplay between autophagy and apoptosis through shared signaling pathways complicates our understanding of how NSCLC pathophysiology is regulated. The apoptotic effect of autophagy is controversial as both inhibitory and stimulatory effects have been reported in NSCLC. In addition, crosstalk of proteins regulating both autophagy and apoptosis exists. Here, we review the recent advances of the relationship between autophagy and apoptosis in NSCLC, aiming to provide few insights into the discovery of novel pathogenic factors and the development of new cancer therapeutics.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms18020367