- Author:
Bo LIU
1
;
Jin-Ku BAO
;
Jin-Ming YANG
;
Yan CHENG
Author Information
- Publication Type:Journal Article
- MeSH: Antibiotics, Antineoplastic; therapeutic use; Apoptosis Regulatory Proteins; metabolism; Autophagy; drug effects; genetics; Beclin-1; Chloroquine; therapeutic use; Drug Discovery; Humans; Membrane Proteins; metabolism; Molecular Targeted Therapy; Neoplasms; metabolism; pathology; therapy; Phosphatidylinositol 3-Kinases; antagonists & inhibitors; metabolism; Signal Transduction; Sirolimus; therapeutic use; TOR Serine-Threonine Kinases; metabolism; Tumor Suppressor Protein p53; metabolism
- From:Chinese Journal of Cancer 2013;32(3):113-120
- CountryChina
- Language:English
- Abstract: Autophagy, an evolutionarily conserved lysosomal degradation process, has drawn an increasing amount of attention in recent years for its role in a variety of human diseases, such as cancer. Notably, autophagy plays an important role in regulating several survival and death signaling pathways that determine cell fate in cancer. To date, substantial evidence has demonstrated that some key autophagic mediators, such as autophagy-related genes (ATGs), PI3K, mTOR, p53, and Beclin-1, may play crucial roles in modulating autophagic activity in cancer initiation and progression. Because autophagy-modulating agents such as rapamycin and chloroquine have already been used clinically to treat cancer, it is conceivable that targeting autophagic pathways may provide a new opportunity for discovery and development of more novel cancer therapeutics. With a deeper understanding of the regulatory mechanisms governing autophagy, we will have a better opportunity to facilitate the exploitation of autophagy as a target for therapeutic intervention in cancer. This review discusses the current status of targeting autophagic pathways as a potential cancer therapy.