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The Inhibitory Effect of Sulforaphane on The Proliferation of Acute Myeloid Leukemia Cell Lines through Controlling
Mohsen Koolivand1, Maryam Ansari2,3, Soheila Moein4
1Royan Stem Cell Technology Company, Tehran, Iran.
Objective:
The present study investigated the role of miR-181a as a small non-coding RNA molecule in acute myeloid leukemia (AML) pathogenesis and reflected on the effects of Sulforaphane (SFN) on AML progression.
Materials And Methods:
This experimental study had two parts. In vivo study, the miR-181a levels was measured in patients with symptoms of AML and compared to healthy controls (HCs) to investigate its role in AML pathogenesis. Afterward, an in vitro study was performed to examine the effects of SFN on the growth, apoptosis and proliferation rate of AML cell lines. Finally, the effect of SFN on miR-181a was evaluated as a major miRNA involved in hematopoiesis.
Results:
The results of this study showed an increasing trend (2.9-fold, P=0.0019) in miR-181a expression levels in AML patients as compared with HCs. The data associated with MTT assay and flow cytometry (FCM) additionally demonstrated the anti-proliferative effects of SFN against AML cell lines, with a reduction in miR-181a levels. As well, no significant difference was noted between 24 hours and 48 hours treatments by SFN. It was deduced that modulation of miR-181a expression levels could be one of the mechanisms associated with the anti-proliferative effects of SFN against AML.
Conclusion:
MiR-181a levels contribute to AML pathogenesis and thus they can be considered as a strategy in controlling AML progression in patients. Accordingly, SFN can arrest cell proliferation and induce apoptosis in AML cell lines through retardation expression of miR-181a and affecting miR-181a pathway, which already clarified its role in the differentiation of hematopoietic stem cells and indicates another mode of anti-cancer action of sulforaphane.
Insights
MicroRNA-181a (miR-181a) levels are elevated in acute myeloid leukemia (AML). Sulforaphane (SFN) reduces AML cell proliferation and miR-181a expression, suggesting a therapeutic strategy.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- Acute myeloid leukemia (AML) is a hematological malignancy with complex pathogenesis.
- MicroRNAs (miRNAs) play crucial roles in cancer development and progression.
- miR-181a is implicated in hematopoiesis and has been linked to various cancers.
Purpose of the Study:
- To investigate the role of miR-181a in AML pathogenesis.
- To evaluate the effects of Sulforaphane (SFN) on AML cell growth, apoptosis, and proliferation.
- To determine if SFN affects miR-181a expression in AML.
Main Methods:
- In vivo study comparing miR-181a levels in AML patients and healthy controls.
- In vitro experiments assessing SFN's impact on AML cell lines using MTT assays and flow cytometry.
- Analysis of SFN's effect on miR-181a expression levels.
Main Results:
- miR-181a expression was significantly increased (2.9-fold) in AML patients compared to healthy controls.
- SFN demonstrated anti-proliferative effects on AML cell lines.
- SFN treatment led to a reduction in miR-181a levels in AML cells.
- No significant difference in SFN efficacy was observed between 24 and 48-hour treatment periods.
Conclusions:
- Elevated miR-181a levels are associated with AML pathogenesis and may serve as a therapeutic target.
- SFN inhibits AML cell proliferation and induces apoptosis, partly by downregulating miR-181a expression.
- SFN's anti-cancer action in AML may involve modulation of the miR-181a pathway, impacting hematopoietic stem cell differentiation.
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