Targeting the stress support network regulated by autophagy and senescence for cancer treatment.
Autophagy and cellular senescence are two potent tumor suppressive mechanisms activated by various cellular stresses, including the expression of activated oncogenes. However, emerging evidence has also indicated their pro-tumorigenic activities, strengthening the case for the complexity of tumorigenesis. More specifically, tumorigenesis is a systemic process emanating from the combined accumulation of changes in the tumor support pathways, many of which cannot cause cancer on their own but might still provide excellent therapeutic targets for cancer treatment. In this review, we discuss the dual roles of autophagy and senescence during tumorigenesis, with a specific focus on the stress support networks in cancer cells modulated by these processes. A deeper understanding of such context-dependent roles may help to enhance the effectiveness of cancer therapies targeting autophagy and senescence, while limiting their potential side effects. This will steer and accelerate the pace of research and drug development for cancer treatment.
['Kim|Jaejin|J|', 'Lee|Yeonghyeon|Y|', 'Roh|Kyeonghwan|K|', 'Kim|Mi-Sung|MS|', 'Kang|Chanhee|C|']
D001343:Autophagy D063646:Carcinogenesis D016922:Cellular Senescence D004249:DNA Damage D053263:Gene Regulatory Networks D006801:Humans D053858:Metabolic Networks and Pathways D058990:Molecular Targeted Therapy D009369:Neoplasms D013312:Stress, Physiological
Autophagy Cellular senescence Tumorigenesis SASP Selective autophagy Senolytics Senostatics Stress support pathway