摘要
Autophagy is a basic catabolic process closely asso-ciated with degradation of cellular components. The role of autophagy in colorectal cancer(CRC) remains controversial. The mechanism of autophagy has been identified as protecting mechanism against tumorige-nesis by isolation of damaged organelles or as cytopro-tective provides energy in hypoxic regions of CRC tumors. Mutations in proto-oncogenes, such as RAS and BRAF, have been associated with autophagy initiation through signaling pathways of BRAF/MEK/ERK and PI3 K/AKT/m TOR. A combination therapy of chemotherapeutic agents and autophagy inhibitors such as hydroxychloroquine or immunotherapy might represent a major step that could be evaluated as a putative novel therapeutic strategy in CRC patients.
Autophagy is a basic catabolic process closely asso-ciated with degradation of cellular components. The role of autophagy in colorectal cancer(CRC) remains controversial. The mechanism of autophagy has been identified as protecting mechanism against tumorige-nesis by isolation of damaged organelles or as cytopro-tective provides energy in hypoxic regions of CRC tumors. Mutations in proto-oncogenes, such as RAS and BRAF, have been associated with autophagy initiation through signaling pathways of BRAF/MEK/ERK and PI3 K/AKT/m TOR. A combination therapy of chemotherapeutic agents and autophagy inhibitors such as hydroxychloroquine or immunotherapy might represent a major step that could be evaluated as a putative novel therapeutic strategy in CRC patients.