GANT61 surmounts drug resistance of ADR by upregulating lysosome activities and reducing BCL2 expression in HL-60/ADR cells.

ABSTRACT:

Background

Drug resistance remains a significant obstacle to Acute myeloid leukemia (AML) successful treatment, often leading to therapeutic failure. Our previous studies demonstrated that Glioma-associated oncogene-1 (GLI1) reduces chemotherapy sensitivity and promotes cell proliferation in AML cells. GANT61, an inhibitor of GLI1, emerges as a promising candidate in AML treatment. This study aims to explore the effects of the combination of GANT61 and Adriamycin (ADR) on AML cells resistance and elucidate the mechanisms through which GANT61 may potentiate the sensitivity of AML cells to ADR.

Methods

AML cell lines and AML primary cells were studied to evaluate effects and mechanisms of GANT61. Flow cytometry assays were used to verify apoptosis. Cell Counting Kit-8 (CCK-8)

SUBMITTER: Zhou C 

PROVIDER: S-EPMC11674180 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature