Friedelin inhibits the growth and metastasis of human leukemia cells via modulation of MEK/ERK and PI3K/AKT signalling pathways

Purpose: Leukemia constitutes just 3% of all malignancies but because of its high incidence and mortality in children and persons below 40 years of age, it is considered one of the devastating malignant conditions. This study was undertaken to evaluate the Anticancer effects of Friedelin triterpenoid against the human AML-196leukemia cells.

Methods: CCK-8 assay was used to determine cell viability. DAPI staining was used for the assessment of Apoptosis. Annexin V/propidium iodide (PI) analysis was employed for the detection of percentage of Apoptosis. Transwell assays were used for cell migration and invasion. Western blotting was used for the determination of protein expression.

Results: The results showed Friedelin inhibited the proliferation of the human AML-196 cells with little effects on the normal cells. Investigation of the underlying mechanisms showed that Friedelin induced Apoptosis in AML-196 cells. Friedelin-induced Apoptosis was linked with upregulation of cleaved Caspase-3, 8 and 9, as well as cleaved PARP. The Bax protein levels were increased and of Bcl-2 were decreased. Transwell assays showed that Friedelin suppressed the migration and invasion of the AML-196leukemia cells. Additionally, Friedelin also blocked the MEK/ERK and PI3K/AT signalling cascades dose-dependently.

Conclusion: Taken together, Friedelin may prove beneficial in the treatment of leukemia.