Glucose transporter‑1 inhibition overcomes imatinib resistance in gastrointestinal stromal tumor cells.

ABSTRACT: Imatinib mesylate (imatinib) is the primary agent of choice used to treat gastrointestinal stromal tumors (GIST). However, drug resistance to imatinib poses a major obstacle to treatment efficacy. In addition, the relationship between imatinib resistance and glycolysis is poorly understood. Glucose transporter (GLUT)‑1 is a key component of glycolysis. The present study aimed to assess the potential relationship between components in the glycolytic pathway and the acquisition of imatinib resistance by GIST cells, with particular focus on GLUT‑1. An imatinib‑resistant GIST cell line was established through the gradual and continuous imatinib treatment of the parental human GIST cell line GIST‑T1. The expression of glycolysis‑related molecules (GLUT‑1, hexokinase 2, pyruvate kinase M2 and la

SUBMITTER: Shima T 

PROVIDER: S-EPMC8600406 | biostudies-literature | 2022 Jan

REPOSITORIES: biostudies-literature