- Author:
Jun-Lin LI
1
;
Shao-Liang HAN
;
Xia FAN
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents; pharmacology; therapeutic use; Apoptosis; drug effects; Autophagy; drug effects; Cell Transformation, Neoplastic; drug effects; Drug Resistance, Neoplasm; Humans; Molecular Targeted Therapy; NF-kappa B; pharmacology; Neoplasms; drug therapy; metabolism; pathology; Proto-Oncogene Proteins c-bcl-2; pharmacology; Signal Transduction; Tumor Microenvironment; Tumor Suppressor Protein p53; pharmacology
- From:Chinese Journal of Cancer 2011;30(10):655-668
- CountryChina
- Language:English
- Abstract: Autophagy is a process in which long-lived proteins, damaged cell organelles, and other cellular particles are sequestered and degraded. This process is important for maintaining the cellular microenvironment when the cell is under stress. Many studies have shown that autophagy plays a complex role in human diseases, especially in cancer, where it is known to have paradoxical effects. Namely, autophagy provides the energy for metabolism and tumor growth and leads to cell death that promotes tumor suppression. The link between autophagy and cancer is also evident in that some of the genes that regulate carcinogenesis, oncogenes and tumor suppressor genes, participate in or impact the autophagy process. Therefore, modulating autophagy will be a valuable topic for cancer therapy. Many studies have shown that autophagy can inhibit the tumor growth when autophagy modulators are combined with radiotherapy and/or chemotherapy. These findings suggest that autophagy may be a potent target for cancer therapy.

