Autophagy-dependent cancer cells circumvent loss of the upstream regulator RB1CC1/FIP200 and loss of LC3 conjugation by similar mechanisms.

ABSTRACT: Macroautophagy/autophagy degrades proteins and organelles to generate macromolecular building blocks. As such, some cancer cells are particularly dependent on autophagy. In a previous paper, we found that even highly autophagy-dependent cancer cells can adapt to circumvent autophagy inhibition. However, it remains unclear if autophagy-dependent cancer cells could survive the complete elimination of autophagosome formation. We extended our previous findings to show that knockout (KO) of both the upstream autophagy regulator RB1CC1/FIP200 and the downstream regulator and mediator of LC3 conjugation, ATG7, strongly inhibits growth in highly autophagy-dependent cells within one week of editing. However, rare clones survived the loss of ATG7 or RB1CC1 and maintained

SUBMITTER: Towers CG 

PROVIDER: S-EPMC7469620 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature