Suppression of Autophagy Can Augment PIK3 Inhibitor Induced Apoptosis in T Lymphoblastic Leukemia Cell Lines

Ann Clin Lab Sci. 2023 Jul;53(4):598-606.

Abstract

Objective: The present study aimed to investigate the effects of the PI3K inhibitor PX-866 or PI-103 combined with the autophagy inhibitor 3-methyladenine (3-MA) on the apoptosis of T lymphoblastic leukemia cells.

Methods: The proliferation and apoptosis of T lymphoblastic leukemia cell lines were detected by CCK-8 and flow cytometer. The expression of proteins was measured by western blot. The effect of PI3K inhibitors combined with 3-MA on the number of autophagosomes was detected by transmission electron microscopy (TEM).

Results: We found PX-866 and PI-103 treatment reduced cell viability while increasing apoptosis in CCRF-CEM and Jurkat cells, which was further enhanced when combined with 3-MA. The phosphorylation levels of AKT and mTOR were suppressed by PX-866 or PI-103, which were reversed by 3-MA. Further, the expression of LC3, ATG5, ATG12 and Beclin-1 was upregulated by PX-866 or PI-103 and downregulated by 3-MA. TEM results revealed that the number of autophagosome was increased by PX-866 or PI-103 treatment, which was reversed by 3-MA.

Conclusions: The results demonstrated that 3-MA could suppress PI3K inhibitor-mediated activation of autophagy to promote the apoptosis of tumor cells. This discovery provided experimental support for constituting a promising strategy for T-cell acute lymphoblastic leukemia (T-ALL) therapy.

Keywords: PI3K inhibitor; T lymphoblastic leukemia/lymphoma; apoptosis; autophagy inhibitor.

MeSH terms

  • Apoptosis
  • Autophagy
  • Cell Line
  • Humans
  • Lymphoma, Non-Hodgkin*
  • Phosphatidylinositol 3-Kinases
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma* / drug therapy

Substances

  • Phosphatidylinositol 3-Kinases