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Open AccessReview

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

1
Department of Molecular and Cellular Biology, University of Arizona, Tucson, AZ 85721, USA
2
Department of Obstetrics and Gynecology, Dong’e No. 4 People’s Hospital, Liaocheng 252200, China
3
Department of Medicine, Division of Hematology-Oncology, Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL 33136, USA
4
Department of Chemical and Life Science Engineering, Virginia Commonwealth University, Richmond, VA 23284, USA
5
Department of Clinical Oncology, Queen Elizabeth Hospital, Kowloon, Hong Kong, China
*
Authors to whom correspondence should be addressed.
Academic Editor: Anthony Lemarié
Int. J. Mol. Sci. 2017, 18(2), 367; https://doi.org/10.3390/ijms18020367
Received: 6 December 2016 / Revised: 22 January 2017 / Accepted: 3 February 2017 / Published: 10 February 2017
(This article belongs to the Collection Advances in Molecular Oncology)
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. View Full-Text
Keywords: non-small-cell lung cancer (NSCLC); apoptosis; autophagy; crosstalk; p53; mammalian target of rapamycin (mTOR); endoplasmic reticulum (ER) stress non-small-cell lung cancer (NSCLC); apoptosis; autophagy; crosstalk; p53; mammalian target of rapamycin (mTOR); endoplasmic reticulum (ER) stress
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MDPI and ACS Style

Liu, G.; Pei, F.; Yang, F.; Li, L.; Amin, A.D.; Liu, S.; Buchan, J.R.; Cho, W.C. Role of Autophagy and Apoptosis in Non-Small-Cell Lung Cancer. Int. J. Mol. Sci. 2017, 18, 367. https://doi.org/10.3390/ijms18020367

AMA Style

Liu G, Pei F, Yang F, Li L, Amin AD, Liu S, Buchan JR, Cho WC. Role of Autophagy and Apoptosis in Non-Small-Cell Lung Cancer. International Journal of Molecular Sciences. 2017; 18(2):367. https://doi.org/10.3390/ijms18020367

Chicago/Turabian Style

Liu, Guangbo; Pei, Fen; Yang, Fengqing; Li, Lingxiao; Amin, Amit D.; Liu, Songnian; Buchan, J. R.; Cho, William C. 2017. "Role of Autophagy and Apoptosis in Non-Small-Cell Lung Cancer" Int. J. Mol. Sci. 18, no. 2: 367. https://doi.org/10.3390/ijms18020367

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Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

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