Targeted therapy for drug-tolerant persister cells after imatinib treatment for gastrointestinal stromal tumours.

ABSTRACT:

Background

Despite the effectiveness of tyrosine kinase inhibitors (TKI), gastrointestinal stromal tumours (GIST) develop after the withdrawal of TKI. Based on previous studies, a subpopulation of drug-tolerant cells called "persister cells" may be responsible for the recurrence and have thus, gained attention as a novel target in cancer therapy.

Methods

The metabolic changes were investigated in imatinib-derived persister GIST cells. We investigated the efficacy and the mechanism of GPX4 inhibitor, which is known as a major inducer of "ferroptosis". We also evaluated the effects of RSL3 to the gefitinib-derived persister lung cancer cells.

Results

We demonstrated a downregulation of glucose metabolism, subsequent decrease in the glutathione level and sensitivity to g

SUBMITTER: Ishida T 

PROVIDER: S-EPMC8608810 | biostudies-literature | 2021 Nov

REPOSITORIES: biostudies-literature