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.
Highlights
Lung cancer is one of the leading causes of all cancer-related deaths
epidermal growth factor receptor (EGFR) abnormalities act through the PI3K/AKT/Mammalian Target of Rapamycin (mTOR) and Raf/MEK/ERK pathways to drive oncogenesis and are discussed below
Platycodin-D, a triterpene saponin extracted from the root of platycodon grandiflorum, induces autophagy in both H460 and A549 Non-small-cell lung cancer (NSCLC) cells exhibited by up-regulation of ATG3, ATG7, Beclin-1 and LC3-II, indicating the autophagic regulation effect of Chinese medicine [179]
Summary
Lung cancer is one of the leading causes of all cancer-related deaths. About 1.6 million people died from lung cancer in 2012, which accounts for 19% of all cancer death worldwide. NSCLC is further divided into three main histological subtypes including squamous-cell carcinoma, adenocarcinoma, and large-cell carcinoma. Autophagy and apoptosis play an important role during lung cancer progression. Apoptosis is regulated by intracellular and/or extracellular signals and characterized by morphological changes of the cell targeted for death that include nuclear fragmentation and condensation, mitochondrial outer membrane permeabilization (MOMP), membrane blebbing, cell shrinkage and apoptotic body formation [7]. Autophagy can play a positive and negative role in promoting apoptosis in NSCLC. Autophagy is always inhibited by different oncoproteins, such as AKT, PI3K, Bcl-1 and mutant p53, which may prevent excessive protein degradation in starved or stressed tumor cells. Persistent activation of autophagy causes autophagic programmed cell death or apoptosis [18,19]. The processes of autophagy and apoptosis are discussed in detail below
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