title: Role of Autophagy and Apoptosis in Non-Small-Cell Lung Cancer.
abstract: 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.
authors.affiliation: Department of Molecular and Cellular Biology, University of Arizona, Tucson, AZ 85721, USA. guangboliu@email.arizona.edu.
authors.forename: Guangbo
authors.initials: G
authors.lastname: Liu
authors.affiliation: Department of Molecular and Cellular Biology, University of Arizona, Tucson, AZ 85721, USA. peifen1990@gmail.com.
authors.forename: Fen
authors.initials: F
authors.lastname: Pei
authors.affiliation: Department of Obstetrics and Gynecology, Dong'e No. 4 People's Hospital, Liaocheng 252200, China. yfqldz@gmail.com.
authors.forename: Fengqing
authors.initials: F
authors.lastname: Yang
authors.affiliation: Department of Medicine, Division of Hematology-Oncology, Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL 33136, USA. lingxiaoli@med.miami.edu.
authors.forename: Lingxiao
authors.initials: L
authors.lastname: Li
authors.affiliation: Department of Medicine, Division of Hematology-Oncology, Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL 33136, USA. amitdipakamin@med.miami.edu.
authors.forename: Amit Dipak
authors.initials: AD
authors.lastname: Amin
authors.affiliation: Department of Chemical and Life Science Engineering, Virginia Commonwealth University, Richmond, VA 23284, USA. sliu6@vcu.edu.
authors.forename: Songnian
authors.initials: S
authors.lastname: Liu
authors.affiliation: Department of Molecular and Cellular Biology, University of Arizona, Tucson, AZ 85721, USA. rbuchan@email.arizona.edu.
authors.forename: J Ross
authors.initials: JR
authors.lastname: Buchan
authors.affiliation: Department of Clinical Oncology, Queen Elizabeth Hospital, Kowloon, Hong Kong, China. chocs@ha.org.hk.
authors.forename: William C
authors.initials: WC
authors.lastname: Cho
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D001343:Autophagy / Q000187:drug effects / Q000235:genetics; D002289:Carcinoma, Non-Small-Cell Lung / Q000235:genetics / Q000378:metabolism* / Q000628:therapy; D002450:Cell Communication; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects; D004734:Energy Metabolism; D014644:Genetic Variation; D006801:Humans; D007167:Immunotherapy; D008175:Lung Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000628:therapy; D020935:MAP Kinase Signaling System; D058990:Molecular Targeted Therapy; D011485:Protein Binding; D012307:Risk Factors; D015398:Signal Transduction; D013312:Stress, Physiological; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism
chemical_list: D051017:Apoptosis Regulatory Proteins; D058570:TOR Serine-Threonine Kinases
keywords: apoptosis; autophagy; crosstalk; endoplasmic reticulum (ER) stress; mammalian target of rapamycin (mTOR); non-small-cell lung cancer (NSCLC); p53