Title:Flavonoid Kaempferol Inhibits the Proliferation and Survival of Human Leukemia HL60 Cells
Volume: 16
Issue: 4
Author(s): Saleheh Rezapour, Elham Hosseinzadeh, Afsaneh Jahangiryan, Behnam Emamgolizade Gurd Tapeh, Nasrin Beheshtkhoo, Mohammad Amin Jadidi Kouhbanani, Ali Hassanzadeh and Faroogh Marofi*
Affiliation:
- Department of Immunology, Division of Hematology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz,Iran
Keywords:
Kaempferol (Kae), acute myeloid leukemia (AML), proliferation, apoptosis, HL60 cells, real-time PCR.
Abstract:
Background: Acute myeloid leukemia (AML) is an aggressive type of leukemia adversely
affecting the normal differentiation and proliferation process of human hematopoietic myeloid lineage.
Over the last decades, Kaempferol (Kae) (3,4′,5,7-tetrahydroxyflavone) has been considered a flavonoid
with useful medical significance, capable of inhibiting various types of leukemia (e.g., AML).
Objective: This study aimed to evaluate the Kae effect on proliferation and apoptosis of a human
AML cell line, HL60.
Methods: The proliferation capability of the HL60 cells was estimated by MTT assay at 12, 24, and
48 hours after exposure to Kae at a series of concentrations, including 10, 25, 50, and 75 μM. Also,
the apoptosis level of HL60 cells was measured 48 hours after exposure to various concentrations of
Kae (10, 25, and 50 μM) using Annexin-V/PI staining and FACS analysis. Besides, the gene expression
of CDK1/2, Bcl-2, survivin, c-FLIP, Mcl-1, XIAP, Bax, and caspase 3 and 8 was assessed following
treatment of HL60 cells with Kae (25 and 50 μM) by Real-Time PCR.
Results: The anti-proliferation activity of Kae showed an ascending pattern over time and reached the
maximum level at 48 hours of HL60 cells exposure to Kae. Also, it was able to trigger apoptosis of
HL60 cells, in particular, at 50 μM concentration. On the other hand, Kae could modify the expression
levels of the candidate’s genes in treated cells.
Conclusion: The promising results of using Kae against the HL60 cells have made it a good drug candidate
to treat AML through up-regulation of caspases expression and down-regulation of antiapoptotic
proteins.
