drug-resistance
Autophagic flux refers to the complete, dynamic throughput of the autophagy pathway — from autophagosome formation, through maturation and fusion with lysosomes, to degradation of their contents — as opposed to a static snapshot of autophagosome number at one point in time. It is commonly assessed via conversion of LC3-I to the lipidated, membrane-associated LC3-II, turnover of the selective autophagy substrate p62/SQSTM1, and phosphorylation of the autophagy-initiating protein Beclin1. Elevated autophagic flux can act as a protective, pro-survival mechanism that helps cancer cells withstand cytotoxic drug treatment.
Related terms
Source papers
- The CAGE–miR-181b-5p–S1PR1 Axis Regulates Anticancer Drug Resistance and Autophagy in Gastric Cancer Cells doi:10.3389/fcell.2021.666387
- Cancer/testis antigen CAGE mediates osimertinib resistance in non-small cell lung cancer cells and predicts poor prognosis in patients with pulmonary adenocarcinoma doi:10.1038/s41598-023-43124-8
- HDAC9 and miR-512 Regulate CAGE-Promoted Anti-Cancer Drug Resistance and Cellular Proliferation doi:10.3390/cimb46060311
- Parkin Induces Ubiquitination and Large Extracellular Vesicle Release of HMGB1 to Activate Antitumor Immunity doi:10.1158/0008-5472.CAN-25-0904